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Hand-washing resistant bacteria. Will they evolve one day?

Hand-washing resistant bacteria. Will they evolve one day?


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I know that soap kills bacteria by dissolving their membrane. But it is not 100% effective. A small portion of bacteria which survive replicates and I have to wash my hands again.

Will this cycle lead to evolution of soap-resistant bacteria with insoluble membranes?


soap isn't a germ killer.

soap is a germ REMOVER. it is basically made of things a lot like phospholipids, that bury their fat loving tails into germs, and their water loving heads stick into the water, making whatever is in the capsule called a "micelle" super slippery,and they wash away.

the cool thing about this is it removes even non living gunk (sometimes).


Not all soap kills bacteria, not all soaps work the same

actually, the rinsing, rubbing, and temperature of the water significantly contribute the removal and termination of bacteria even then this is not 100%.

I wouldn't want to touch blood with AIDS virus or Ebola and rely solely on soap and hand washing to save the day.

Some soaps work by raising the PH and there are already a category of organisms called Alkaliphiles which thrive in high PH environments. To my knowledge these cant really harm you as you are a low PH organism.

But yes theoretically if you use the same measure against a bacterium long enough and constantly give it a chance to succeed, eventually it will.


Hand-washing resistant bacteria. Will they evolve one day? - Biology

Phylogenetic modeling concepts are constantly changing. It is one of the most dynamic fields of study in all biology. Over the last several decades, new research has challenged scientists’ ideas about how organisms are related. The scientific community has proposed new models of these relationships.

Many phylogenetic trees are models of the evolutionary relationship among species. Phylogenetic trees originated with Charles Darwin, who sketched the first phylogenetic tree in 1837 (Figure 1a). This served as a prototype for subsequent studies for more than a century. The phylogenetic tree concept with a single trunk representing a common ancestor, with the branches representing the divergence of species from this ancestor, fits well with the structure of many common trees, such as the oak (Figure 1b). However, evidence from modern DNA sequence analysis and newly developed computer algorithms has caused skepticism about the standard tree model’s validity in the scientific community.

Figure 1. The (a) concept of the “tree of life” goes back to an 1837 sketch by Charles Darwin. Like an (b) oak tree, the “tree of life” has a single trunk and many branches. (credit b: modification of work by “Amada44″/Wikimedia Commons)


Biology_Unit 11_Quiz 1: Animal Behaviors. NOTES.

1.What mechanisms are causing the behavior?
2.How does the behavior develop?
3. What is its survival value?
4.How did it evolve?

Keep in mind that this doesn't mean that because a child's parents are shy, there is a shy gene passed down to make the child shy as well. The child could learn the shy behavior by simply observing and emulating this behavior. There always seems to be a combination of both nature and nurture in influencing behavior.

Evolution. Evolution is based on genetic inheritance. A change in the genotype of an organism is passed down from parent to offspring again and again. Over time, the genes in a population change and the phenotype of an organism is altered. Animals seem to evolve in a way that best helps them to survive or adapt to their environment. Imagine a population of jaguars. Some are fast runners, which allows them to easily catch prey. The rest of the jaguars are slow runners, which makes it more difficult to catch prey. Since they do not catch prey as easily, the slow jaguars die more often than the fast jaguars because they cannot eat. The slow jaguars also reproduce less often than the fast jaguars. Since more fast jaguars reproduce than slow jaguars, most offspring inherit the gene for fast running. This favorable gene is continually passed down from parent to offspring.
This example is similar to the passing on of behaviors, and how behaviors evolve due to the greatest fitness for the species. This is called the optimality theory. If a behavior benefits a species more than it costs the species, it will be repeated and passed on for generations. Thus, each species has its own unique evolutionary history in behavior as well as in its evolutionary history of anatomy and physiology.
Physiology. What are our physiological needs? In order to function properly, we need to eat, sleep, drink, breathe, etc. How does your behavior change if you don't meet a physiological need? If you don't eat, you might become grumpy. Some people may even steal in order to feed themselves. Animals are similar. Their basic needs must be met as well, and their behavior coincides with getting these needs met. Although all organ systems are involved in producing a behavior, the nervous and endocrine systems have the most influence. The nervous system is the communicator of the body. It receives a stimulus and directs a response. The endocrine system produces hormones that also communicate with different parts of the body. The relationship of the endocrine system is commonly seen when it's time for animals to mate or breed. For example, male sheep get along well with other males until mating season. At this time, their reproductive organs drop, sperm are produced, and male hormones are activated. This, in turn, affects the animal's physiology and behavior. The male sheep are now territorial and fight other males to attract females.

Habituation. Tube worms instinctively cringe into their tube when a shadow passes over them. This is because the shadow often belongs to a predator. However, place this worm in a controlled environment where a shadow is cast over it without any consequence, and the worm will learn that there is no threat and stop hiding. Habituation is learning not to continue a behavior due to a lack of reinforcement for that behavior.

Classical conditioning. Pavlov's experiment is a typical case of classical conditioning in which an instinctive response or behavior to a stimulus is learned for a different stimulus. The dog's instinctive behavior is to salivate to food. The dog was conditioned to associate a bell with food because every time a bell rang, food was presented. So the dog began to salivate not just to food, but to a different stimulus—a bell.

Operant conditioning. If you give a dog a treat every time you tell it to sit, it will continue to sit when asked. This is the basis of operant conditioning in which a learned behavior becomes more frequent or infrequent due to rewards or consequences. An experiment was conducted in which a hungry rat was placed in a box. The rat crawled and sniffed all over the box, exploring it. During this exploration, it discovered a button in the box that distributed food if it was pressed. The rat began to push the button more frequently and then more exclusively anytime it wanted a piece of food. It was conditioned to learn that if it pushed the button, it would receive a reward—food.

Latent learning. Animals can learn without reward or reinforcement. Latent learning is when an animal learns a new behavior without receiving an immediate reward. In fact, the discovery or information learned may not be expressed until a situation calls for it. It's like watching your dad tighten a screw. Later in life, you may find a loose screw, grab a screwdriver and tighten it, just like your dad did, without any additional instruction needed. Simple exploration by the animal is often the example used with latent learning. For example, a hollow piece of wood was placed in a chipmunk's habitat. The chipmunk sniffed and explored the wood and then went on its way. A cat was then placed in the chipmunk's area. The chipmunk ran directly to the wood and hid beneath it.

Insightful learning. Insightful learning seems to be a more complex learning ability. It involves problem solving, insight, and planning. An experiment was done with monkeys. The monkeys were placed in a cage full of different toys like crates and sticks. Bananas were hung near the cage but out of the monkeys' reach. After many attempts to reach the bananas, the monkeys became frustrated and finally gave up. Then the monkeys noticed the toys available to them. They explored the different toys, and some attempted to stack the crates to reach the bananas others tried to reach the bananas with a stick. One found a way to attach two sticks together so it was long enough to reach the bananas. Insightful learning is a sudden appearance of different behaviors that solve a once unsolvable problem.

Social learning. We have all picked up habits or learned a behavior by watching and doing as others do. That is the basis of social learning. Social learning occurs automatically with many offspring. Newborn animals spend a lot of time with their parents, following them around and watching how to hunt and where to find food and water, etc. If you set a bird feeder out in your backyard, birds won't come and start feeding right away. But once one or two discover the bird feeder and start to feed, more birds then come. This is because other birds are watching and learning from the others.

Behavior in movement. A major difference between plants and animals is that animals move from place to place. They move to satisfy physiological needs. Roly-poly bugs, for instance, thrive in moist conditions. They'll move around in no particular direction till they find a wet spot and then stay there. This simple movement is called kineses and is mainly due to environmental conditions. Some animals, like moths or earthworms, move toward or away from light sources. Movement based on a stimulus is called taxis. It is similar to tropisms in plants. Like phototropism, phototaxis is when an animal's movement is toward or away from a light source. A type of movement by animals you may be more familiar with is migration. Periodically, animals will move or migrate to a different area to seek food, mates, or shelter. Birds flying south for the winter is an example of a migration. Salmon migrate upstream during a certain season to mate. Many animals migrate for various reasons.

Food search. Animals behave in a certain way to find food. Some are very particular with what they eat others are not. Each has its own way to get food. Filter feeding is done by most aquatic invertebrates, like sponges, and some vertebrates, like the Baleen whale, which swallows huge amounts of water to be filtered for food and nutrients like plankton. Some animals, like herbivores, take advantage of their immobile and plentiful food source—plants. Herbivores can save the energy to hunt or chase after their food source. Carnivores are those animals that eat other animals. Thus, these animals must find and capture prey and avoid being captured themselves unless they're on top of the food chain. The optimality theory of animal behavior suggests that the behaviors which evolve are those that benefit the animal the most. Many predators have the ability to strategize. They need this ability to obtain food. And most predators can assess the environment, choose a prey that is abundant and easy to obtain, and cooperate with others in a capture.

Avoiding capture. Unless an animal is at the top of the food chain, it's at risk for becoming lunch! Thus, most animals must always be on the defense. One way to do this is to avoid being detected. Many animals will freeze up if they hear an unfamiliar sound or feel or smell an approaching predator. Some animals can blend into their settings by the color of their fur or skin, which may change with the seasons. They can resemble other objects, like leaves or twigs of a tree, as well. Animals may have chemical or physical defenses, like the spray from a skunk or the stinger of a wasp.

Some animals employ the use of mimicry to escape predation. In biology, mimicry is the imitating of an organism (the mimic) from another organism (the model). The mimicry of a trait or traits helps the mimic to survive. There are two major types of mimicry, Batesian and Müllerian. In both types of mimicry, one species copies another to escape predation. A harmless moth that resembles a wasp would be an example of Batesian mimicry. The moth is the mimic and the wasp is the model. The nontoxic moth is unable to sting another animal, but mimics the yellow jacket wasp that is able to sting another animal. Müllerian mimicry is one in which both the mimic and the model are both dangerous to the potential predator and there is no distinction between the mimic and the model. An example of this would be the yellow jacket wasp and the bumblebee. Both of the species possess bright yellow and black colors and are able to use their sting as a defense method.

Like the optimality theory suggests, the benefits outweigh the costs, so many animals tend to cooperate with one another to reach the common goal of survival. Cooperation can be within the same species or between organisms of different species. A pack of hyenas, for example, can attack and kill larger prey if they work together than if they try to hunt individually. Similarly, a flock of geese can save energy during migration by flying together. Have you ever run behind someone on a windy day? The person in front of you creates a shield that protects you from the wind, making your run easier. The lead goose in the classic V formation does the same thing. He shields the other geese from the wind, making their flight easier. When the lead goose gets tired, he moves to the back of the formation and another goose takes his place.

Communication. Like in any family, organization, or group, communication is key. Animals communicate in many different ways, with similarities to how humans communicate. While we speak in different human languages, animals have their own language in the noises they may make, like barking, whistling, chirping, or croaking. Noises can attract mates or send out distress or alarm signals to others in the group. While we can communicate nonverbally in our facial expressions, tone, or gestures, animals also make nonverbal physical gestures—for example, a cat warning a dog not to come near it by arching its back, hissing, and showing its teeth. A deer will raise its tail to warn others of a predator. As we can express affection or dislike by physical contact, some animals also communicate by touch, like the social grooming practices of monkeys. In sporting events, we compete against other teams to see who's dominant in the sport. Animals also establish dominance hierarchies by exhibiting physical strength against others. They have leaders, those second in line, those third in line, etc. Some animals use scent or odor to communicate—like a dog marking its territory. Group identity is also exhibited by scent. For instance, an ant that smells different from the other members of a group will be attacked.

Mutualism. In mutualism, both species benefit. The benefits can occur with a resource traded for another resource, like in the example of fungi and orchids. The fungi feed on the roots of the plants, pulling out carbohydrates, while at the same time making nitrogen and phosphates for the plant to use. There is also a resource traded for a service relationship in mutualism. For example, insects and birds receive nectar from flowers, and, as a result, they help conduct pollination for the flower. In some cases, a service-for-service relationship can be seen—like with ants that nest in acacia trees. These ants help protect the tree by attacking herbivores while the nesting grounds in the tree's thorns protect the ants from predators.

Mutualism has significantly contributed to the biodiversity of organisms you see today. Many organisms depend on mutualistic relationships to continue their species.

Commensalism. In commensalism, only one organism benefits, but the other is not harmed. There are many ways in which organisms benefit from commensalism. Some organisms have a special type of commensalism called phoresy. In phoresy, one organism attaches itself to another organism for the purpose of transportation. Barnacles, for example, are marine organisms that cannot move on their own. Instead of remaining in one place, barnacles attach themselves to the shells and skin of other animals. The barnacles gain a mode of transportation, but the other organism gains nothing. Another example of phoresy is the remora fish that attaches itself to sharks. The remora gains transportation and protection from the shark. The shark is not harmed by the relationship, but it is not helped either.

Other organisms benefit from commensalism by gaining access to food. Cattle Egrets are a bird species that live among livestock, such as cattle and horses. The birds feed on insects stirred up by the movement of the grazing animals. The egrets benefit from the relationship, but the livestock do not. Commensalism also helps some plant species spread their seeds. Burdocks are common weeds found in fields and along roadsides. The seed heads of burdocks have long, curved spines, like a fishhook. The hooks catch onto the fur of passing animals and are carried away from the parent plant. When the seed heads fall off, they are able to grow in a new environment.

Do you know anyone who has a hermit crab? Hermit crabs have soft bodies, but they cannot grow their own shells. Instead, they use the shells of dead organisms, such as snails, for protection. Anemonefish, commonly called clownfish, also benefit from the protection of another organism. Clownfish live inside sea anemones. The long, poisonous tentacles of the sea anemone protect the fish from predators. In both situations, one organism benefits, but the other does not.

Biologists argue that true commensalism is rare, if not nonexistent. Most commensal relationships have at least a small effect on the second organism. The organism may appear to be unaffected, but it may be helped or harmed in a subtle way. For example, when barnacles attach to another organism, they add weight. It is not yet known if the extra weight harms the second organism. On the other hand, an organism with barnacles attached to it may be less of a target for a predator. It may actually benefit the organism to have barnacles.

Parasitism. Parasitism is a relationship between two organisms which hurts one and helps the other. The organism that is helped is called the parasite. The organism that is harmed is called the host. In many cases of parasitism, the host is not only hurt, it is killed. A common example of a parasitic relationship is athlete's foot. The athlete's foot fungus grows on a person's skin and may cause serious infection if not treated properly. Other parasitic relationships include lice, ticks, and fleas.

Parasites can live on or in the body of a host. Those that live on the outer body of a host are called ectoparasites and those living inside a host are called endoparasites. A tapeworm is an example of an endoparasite that lives in the intestines of a larger animal. A tick is an example of an ecotoparasite which attaches to the skin of an animal and feeds off the animal's blood.

Most parasites harm their hosts by eating tissue or releasing poisonous chemicals. Have you ever accidentally cut your skin with rusty metal? If so, you probably went to the doctor for a tetanus shot. Bacteria that often live on old metal items secrete chemicals that interfere with nerve impulses in the body.

There are two main types of parasitic relationships. The first is like a hit and run. The parasite lives on the host for a short period of time and then moves on to another organism without killing the first. Ticks are an example of short-term parasitism. The second type of relationship is long-term. The parasite stays with the host until it dies, or until both organisms die. Blood flukes are a type of flatworm that live in the veins of their hosts. The flukes remain with the host until the host dies.

Many biologists believe that parasitism is one of the most powerful forces of evolution. In a parasitic relationship, it is beneficial for both the parasite and the host to evolve and adapt. As adaptations give the host greater protection against the parasite, the parasite also adapts by attacking in new or stronger ways. Have you heard of "super germs"? The term refers to a new strain of antibacterial-resistant bacteria. As humans developed new ways to kill bacteria, the bacteria evolved and are now able to withstand most medications.


Dawn of the superbug: New E. coli strain terrifies scientists

For years experts have warned there would come a day when antibiotics would cease being effective.

And it seems that day could be sooner than first thought after scientists discovered a new superbug that is not just impervious to the last-line-of-defense medication, but has the ability to infect other bacteria.

But instead of destroying its virulent cousins, this new strain of E. coli actually strengthens them by giving them the same antibiotic shield.

The unstoppable superbug was first found in China a few weeks ago.

Chinese and British scientists identified the first strain in a pig, then in raw pork meat and then in a small number of people.

Experts, while worried about the potential effect this discovery would have, hoped it would remain in China.

But this week those hopes were dashed when researchers in Denmark revealed they had found a similar strain in poultry from Germany as well as in a Danish man who had never traveled outside the country.

The superbug has also been found in Malaysia.

Further tests carried out on food samples from 2012 to 2014 by the Technical University of Denmark’s National Food Institute (NFI) in Søborg and the State Serum Institute in Copenhagen found the deadly mutation was present.

This sparked calls from the head of NFI’s genomic epidemiology group, Frank Aarestrup, for other universities with similar databases to carry out testing, online health magazine STAT reported.

What makes this strain different from other E. coli is that it carries a gene named mcr-1.

It is thought this gene is what gives the strain its super-strength and the ability to infect other bacteria.

Dr. Sanjaya Senanayake from ANU College of Medicine, Biology and Environment told news.com.au the Danish discovery was a real worry.

“It was a problem when we heard they were found in China a couple of weeks ago but one had hoped that it would just be in China and wouldn’t spread too quickly but they have now found it in Denmark,” he said. “These are very bad superbugs to have.”

He explained while the risk to Australia was not as serious as other parts of the world, the rate at which the bacteria can spread, and how easily, could be devastating.

“We in Australia are a lot better off than other countries in terms of dealing with resistant bacteria but we are starting to see them come here,” Senanayake said. “The issue of course is Australians travel and when people travel and visit other countries, they drink the water, eat food, walk around and you pick up the local bacteria.

“A number of studies have shown that travelers going to countries that have resistant bacteria in them will often come back with those resistant bacteria sitting in their bowels. If it doesn’t cause an infection, then it’s OK and usually after a few months, they lose that bacteria. But if it does, it can cause serious problems.”

He explained the emergence of medical tourism also posed a risk, adding that hospitals in general are known to have a higher proportion of superbugs.

If a person traveled to a country where the superbug had been found and underwent a procedure in a hospital, he said they had a greater risk of contracting the drug-resistant bug.

Why is the emergence of this superbug such a bad thing?

It basically means the bacteria that causes common gut, urinary and blood infections in humans can now become “pan-resistant” to all antibiotics currently available.

Not only that, but it will make some infections incurable, unless new kinds of antibiotics are developed.

Plus this new strain has the ability to make other bacteria from different families resistant, opening up another can of worms.

How could a potentially deadly super-resistant bacteria evolve?

One of the main theories is the overuse of antibiotics.

While there has been much discussion about the overprescribing of antibiotics by doctors, the bigger concern is the overuse in the agricultural industry.

Since the discovery in Denmark, experts from around the world have begun calling for a ban on the use of the antibiotic colistin in the agricultural industry.

Colistin is an old drug that was rarely used because of the emergence of newer drugs.

But since antibiotic resistance has increased, the need to preserve the drug in the fight against resistance has been imperative. So imperative that in 2012, the World Health Organization designated it as critically important for human medicine, STAT reported.

Despite this, vast quantities of it have been used to help animals grow. In China, the drug is used more in animal production than it is on people, Timothy Walsh, a medical microbiologist from Cardiff University in Wales, told STAT.

“We needed to have definitive borders between antibiotics that are used in human medicine and those that are used in the veterinary sector,” he added.

Senanayake told news.com.au that while the overuse of antibiotics in agriculture is a major factor, so was the overprescribing and overuse by humans.

“Doctors can prescribe antibiotics better, and we have to decide whether we need to give antibiotics, and if we do we should give a narrow antibiotic that doesn’t attack other bacteria,” he explained. “As patients or consumers, we should also decide if we should be asking for an antibiotic at all.

“But one of the bigger factors is that animals consume a lot of antibiotics. In the US, for example, about 80 percent of antibiotics used are used in animals, not humans.

“They are being given to animals to prevent infection but also to promote growth. They think antibiotics help animals grow. This is actually an issue that is being looked at. Vets and doctors are trying to monitor and curb antibiotic use in the animal industry.”

Can it be defeated?

Researchers from the US and Denmark are trying to track its origin, but it is thought it would most likely be China given its prevalent use of colistin.

The bulk of the 12,000 tons of colistin fed to livestock yearly around the world is used in China.

According to New Scientist, antibiotic growth promoters were banned in Europe, and Denmark, ironically, was among the first to ban them.

But in 2013, the European Medicines Agency reported that polymyxins (the group of drug that colistin belongs to) were the fifth most heavily used type of antibiotic in European livestock.

Why not develop more antibiotics?

Senanayake explained that research and development of new antibiotics had actually slowed over the last decade because there were so many already on the market.

But he said there has been a push in recent years by governments, in particular the US, to find more.

“The US government is trying to provide incentives for pharmaceutical companies to make antibiotics,” he explained. “They are doing things like trying to reduce the regulatory burden for them.

“It has been estimated that by 2050, around $100 trillion will be spent on antibiotic-resistant bacteria and there will be about 300 million deaths.

“And even now in the US, they say there are over 2 million illnesses attributed to antibiotic-resistant bacteria and about 23,000 deaths.”

Senanayake said that while developing new antibiotics was one major part of tackling the resistance problem, less prescribing and less reliance was also needed as well as a major rethink of how they are used in the agricultural industry.

“The chief medical officer in the UK recognized antibiotic resistance as a catastrophic threat and wanted it put into the international register of civil emergencies along with terrorism and natural disasters,” he said. “I think that is a positive thing that top people in government are starting to recognize it as a big problem.

“And while it’s not the biggest problem in the world, it certainly is an important problem.”


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Queenan, A. M., Shang, W., Bush, K. & Flamm, R. K. Differential selection of single-step AmpC or efflux mutants of Pseudomonas aeruginosa by using cefepime, ceftazidime, or ceftobiprole. Antimicrob. Agents Chemother. 54, 4092–4097, doi: 10.1128/AAC.00060-10 (2010).

Akasaka, T., Tanaka, M., Yamaguchi, A. & Sato, K. Type II topoisomerase mutations in fluoroquinolone-resistant clinical strains of Pseudomonas aeruginosa isolated in 1998 and 1999: role of target enzyme in mechanism of fluoroquinolone resistance. Antimicrob. Agents Chemother. 45, 2263–2268 (2001).

Higgins, P. G., Fluit, A. C., Milatovic, D., Verhoef, J. & Schmitz, F. J. Mutations in GyrA, ParC, MexR and NfxB in clinical isolates of Pseudomonas aeruginosa. Int. J. Antimicrob. Agents 21, 409–413 (2003).

Jalal, S., Ciofu, O., Høiby, N., Gotoh, N. & Wretlind, B. Molecular mechanisms of fluoroquinolone resistance in Pseudomonas aeruginosa isolates from cystic fibrosis patients. Antimicrob. Agents Chemother. 44, 710–712 (2000).

Li, X. Z., Livermore, D. M. & Nikaido, H. Role of efflux pump(s) in intrinsic resistance of Pseudomonas aeruginosa: resistance to tetracycline, chloramphenicol and norfloxacin. Antimicrob. Agents Chemother. 38, 1732–1741 (1994).

Ojala, V., Laitalainen, J. & Jalasvuori, M. Fight evolution with evolution: plasmid-dependent phages with a wide host range prevent the spread of antibiotic resistance. Evol. Appl. 6, 925–932, doi: 10.1111/eva.12076 (2013).

Zhang, Q. G. & Buckling, A. Phages limit the evolution of bacterial antibiotic resistance in experimental microcosms. Evol. Appl. 5, 575–582, doi: 10.1111/j.1752-4571.2011.00236.x (2012).

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Stamatakis, A. RAxML-VI-HPC: Maximum likelihood-based phylogenetic analyses with thousands of taxa and mixed models. Bioinformatics 22, 2688–2690 (2006).

Yang, Z. PAML: a program package for phylogenetic analysis by maximum likelihood. Comput. Appl. Biosci. 13, 555–556 (1997).


Scientists have found a new strain of bacteria that is resistant to all antibiotics

SCIENTISTS have discovered a strain of bacteria that’s resistant to all antibiotics, sparking a mad scramble for answers.

A life-threatening superbug as viewed under a microscope. Picture: Supplied Source:News Limited

FOR years experts have warned there would come a day when antibiotics would cease being effective.

And it seems that day could be sooner than first thought after scientists discovered a new superbug that is not just impervious to the last line of defence medication, but has the ability to infect other bacteria.

But instead of destroying its virulent cousins this new strain of e.coli actually strengthens them by giving them the same antibiotic shield.

The unstoppable superbug was first found in China a few weeks ago.

Chinese and British scientists identified the first strain in a pig, then in raw pork meat and then in a small number of people.

Experts, while worried about the potential effect this discovery would have, hoped it would remain in China.

But this week those hopes were dashed when researchers in Denmark revealed they had found a similar strain in poultry from Germany as well as in a Danish man who had never travelled outside the country.

The superbug has also been found in Malaysia.

Further tests carried out on food samples from 2012-2014 by the Technical University of Denmark’s National Food Institute in Sྋorg and the State Serum Institute in Copenhagen, found the deadly mutation was present.

This sparked calls from the head of NFI’s genomic epidemiology group, Frank Aarestrup, for other universities with similar databases to carry out testing, online health magazine STAT reported.

What makes this strain different from other e.coli is that it carries a gene named mcr-1.

It is thought this gene is what gives the strain its super-strength and the ability to infect other bacteria.

A poultry farm in Hefei, eastern China's Anhui province is being inspected after the discovery of a deadly and fast-spreading bacteria resistant to last-line antibiotics. Picture: AFP Source:AFP

Dr Sanjaya Senanayake from ANU College of Medicine, Biology and Environment told news.com.au the Danish discovery was a real worry.

“It was a problem when we heard they were found in China a couple of weeks ago but one had hoped that it would just be in China and wouldn’t spread too quickly but they have now found it in Denmark,” he said. “These are very bad superbugs to have.”

He explained while the risk to Australia was not as serious as other parts of the world, the rate at which the bacteria can spread, and how easily, could be devastating.

“We in Australia are a lot better off than other countries in terms of dealing with resistant bacteria but we are starting to see them come here,” Dr Senanayake said. “The issue of course is Australians travel and when people travel and visit other countries, they drink the water, eat food, walk around and you pick up the local bacteria.

𠇊 number of studies have shown that travellers going to countries that have resistant bacteria in them will often come back with those resistant bacteria sitting in their bowels. If it doesn’t cause an infection then it’s OK and usually after a few months they lose that bacteria. But if it does it can cause serious problems.”

He explained the emergence of medical tourism also posed a risk adding that hospitals in general are known to have a higher proportion of superbugs.

If a person travelled to a country where the superbug had been found and underwent a procedure in a hospital, he said they had a greater risk of contracting the drug-resistant bug.

WHY IS THE EMERGENCE OF THIS SUPERBUG SUCH AS BAD THING?

Well, it basically means the bacteria that causes common gut, urinary and blood infections in humans, can now become “pan-resistant” to all antibiotics currently available.

Not only that, but it will make some infections incurable, unless new kinds of antibiotics are developed.

Plus this new strain has the ability to make other bacteria from different families resistant, opening up another can of worms.

The discovery of a new superbug has prompted calls for more antibiotics to be developed. Picture: AFP Martin Bernetti Source:AFP

HOW COULD A POTENTIALLY DEADLY SUPER-RESISTANT BACTERIA EVOLVE?

One of the main theories is the overuse of antibiotics.

While there has been much discussion about the overprescribing of antibiotics by doctors, the bigger concern is the overuse in the agricultural industry.

Since the discovery in Denmark, experts from around the world have begun calling for a ban on the use of the antibiotic colistin in the agricultural industry.

Colistin is an old drug that was rarely used because of the emergence of newer drugs.

But since antibiotic resistance has increased, the need to preserve the drug in the fight against resistance has been imperative. So imperative that in 2012 the World Health Organisation designated it as critically important for human medicine, STAT reported.

Despite this, vast quantities of it have been used to help animals grow. In China, the drug is used more in animal production than it is on people, Timothy Walsh, a medical microbiologist from Cardiff University in Wales, told STAT.

“We needed to have definitive borders between antibiotics that are used in human medicine and those that are used in the veterinary sector,” he added.

Dr Senanayake told news.com.au while the overuse of antibiotics in agriculture is a major factor, so was the overprescribing and over use by humans.

𠇍octors can prescribe antibiotics better, and we have to decide whether we need to give antibiotics, and if we do we should give a narrow antibiotic that doesn’t attack other bacteria,” he explained. 𠇊s patients or consumers we should also decide if we should be asking for an antibiotic at all.

𠇋ut one of the bigger factors is that animals consume a lot of antibiotics. In the US, for example, about 80 per cent of antibiotics used are used in animals not humans.

“They are being given to animals to prevent infection but also to promote growth. They think antibiotics help animals grow. This is actually an issue that is being looked at. Vets and doctors are trying to monitor and curb antibiotic use in the animal industry.”

Researchers from the US and Denmark are trying to track its origin but it is thought it would most likely be China given its prevalent use of colistin.

The bulk of the 12,000 tonnes of colistin fed to livestock yearly around the world is used in China.

According to New Scientist, antibiotic growth promoters were banned in Europe and Denmark, ironically, was among the first to ban them.

But in 2013, the European Medicines Agency reported that polymyxins (the group of drug colistin belongs to) were the fifth most heavily used type of antibiotic in European livestock.

WHY NOT DEVELOP MORE ANTIBIOTICS?

Dr Senanayake explained research and development of new antibiotics had actually slowed over the last decade because there were so many already on the market.

But he said there has been a push in recent years by governments, in particular the US to find more.

“The US government is trying to provide incentives for pharmaceutical companies to make antibiotics,” he explained. “They are doing things like trying to reduce the regulatory burden for them.

“It has been estimated that by 2050 around 100 trillion dollars will be spent on antibiotic resistant bacteria and there will be about 300 million deaths.

𠇊nd even now in the US they say there are over two million illnesses attributed to antibiotic resistant bacteria and about 23,000 deaths.”

Dr Senanayake said while developing new antibiotics was one major part of tackling the resistance problem, less prescribing and less reliance was also needed as well as a major rethink about how they are used in the agricultural industry.

“The chief medical officer in the UK recognised antibiotic resistance as a catastrophic threat and wanted it put into the international register of civil emergencies along with terrorism and natural disasters,” he said. “I think that is a positive thing that top people in government are starting to recognise it as a big problem.

𠇊nd while it’s not the biggest problem in the world it certainly is an important problem.”

For more than a year, Cornell University's Christopher Mason and his team of researchers have been identifying bacteria in the New York City subway system. And some of the fin.

For more than a year, Cornell University's Christopher Mason and his team of researchers have been identifying bacteria in the New York City subway system. And some of the findings might surprise you. Photo: Katie Orlinsky for The Wall Street Journal


20.3 Perspectives on the Phylogenetic Tree

By the end of this section, you will be able to do the following:

  • Describe horizontal gene transfer
  • Illustrate how prokaryotes and eukaryotes transfer genes horizontally
  • Identify the web and ring models of phylogenetic relationships and describe how they differ from the original phylogenetic tree concept

Phylogenetic modeling concepts are constantly changing. It is one of the most dynamic fields of study in all biology. Over the last several decades, new research has challenged scientists’ ideas about how organisms are related. The scientific community has proposed new models of these relationships.

Many phylogenetic trees are models of the evolutionary relationship among species. Phylogenetic trees originated with Charles Darwin, who sketched the first phylogenetic tree in 1837 (Figure 20.12a). This served as a prototype for subsequent studies for more than a century. The phylogenetic tree concept with a single trunk representing a shared ancestry, with the branches representing the divergence of species from this ancestry, fits well with the structure of many common trees, such as the oak (Figure 20.12b). However, evidence from modern DNA sequence analysis and newly developed computer algorithms has caused skepticism about the standard tree model's validity in the scientific community.

Limitations to the Classic Model

Classical thinking about prokaryotic evolution, included in the classic tree model, is that species evolve clonally. That is, they produce offspring themselves with only random mutations causing the descent into the variety of modern-day and extinct species known to science. This view is somewhat complicated in eukaryotes that reproduce sexually, but the laws of Mendelian genetics explain the variation in offspring, again, to be a result of a mutation within the species. Scientists did not consider the concept of genes transferring between unrelated species as a possibility until relatively recently. Horizontal gene transfer (HGT), or lateral gene transfer, is the transfer of genes between unrelated species. HGT is an ever-present phenomenon, with many evolutionists postulating a major role for this process in evolution, thus complicating the simple tree model. Genes pass between species which are only distantly related using standard phylogeny, thus adding a layer of complexity to understanding phylogenetic relationships.

The various ways that HGT occurs in prokaryotes is important to understanding phylogenies. Although at present some do not view HGT as important to eukaryotic evolution, HGT does occur in this domain as well. Finally, as an example of the ultimate gene transfer, some scientists have proposed genome fusion theories between symbiotic or endosymbiotic organisms to explain an event of great importance—the evolution of the first eukaryotic cell, without which humans could not have come into existence.

Horizontal Gene Transfer

Horizontal gene transfer (HGT) is the introduction of genetic material from one species to another species by mechanisms other than the vertical transmission from parent(s) to offspring. These transfers allow even distantly related species to share genes, influencing their phenotypes. Scientists believe that HGT is more prevalent in prokaryotes, but that this process transfers only about 2% of the prokaryotic genome. Some researchers believe such estimates are premature: we must view the actual importance of HGT to evolutionary processes as a work in progress. As scientists investigate this phenomenon more thoroughly, they may reveal more HGT transfer. Many scientists believe that HGT and mutation are (especially in prokaryotes) a significant source of genetic variation, which is the raw material in the natural selection process. These transfers may occur between any two species that share an intimate relationship (Table 20.1).

Mechanism Mode of Transmission Example
Prokaryotes transformation DNA uptake many prokaryotes
transduction bacteriophage (virus) bacteria
conjugation pilus many prokaryotes
gene transfer agents phage-like particles purple non-sulfur bacteria
Eukaryotes from food organisms unknown aphid
jumping genes transposons rice and millet plants
epiphytes/parasites unknown yew tree fungi
from viral infections

HGT in Prokaryotes

HGT mechanisms are quite common in the Bacteria and Archaea domains, thus significantly changing the way scientists view their evolution. The majority of evolutionary models, such as in the Endosymbiont Theory, propose that eukaryotes descended from multiple prokaryotes, which makes HGT all the more important to understanding the phylogenetic relationships of all extant and extinct species. The Endosymbiont Theory purports that the eukaryotes' mitochondria and the green plants' chloroplasts and flagellates originated as free-living prokaryotes that invaded primitive eukaryotic cells and become established as permanent symbionts in the cytoplasm.

Microbiology students are well aware that genes transfer among common bacteria. These gene transfers between species are the major mechanism whereby bacteria acquire resistance to antibiotics. Classically, scientists believe that three different mechanisms drive such transfers.

  1. Transformation: bacteria takes up naked DNA
  2. Transduction: a virus transfers the genes
  3. Conjugation: a hollow tube, or pilus transfers genes between organisms

More recently, scientists have discovered a fourth gene transfer mechanism between prokaryotes. Small, virus-like particles, or gene transfer agents (GTAs) transfer random genomic segments from one prokaryote species to another. GTAs are responsible for genetic changes, sometimes at a very high frequency compared to other evolutionary processes. Scientists characterized the first GTA in 1974 using purple, non-sulfur bacteria. These GTAs, which are most likely derived from bacteriophage DNA inserted in a prokaryote that lost the ability to produce new bacteriophages, carry random DNA pieces from one organism to another. Controlled studies using marine bacteria have demonstrated GTAs' ability to act with high frequency. Scientists have estimated gene transfer events in marine prokaryotes, either by GTAs or by viruses, to be as high as 10 13 per year in the Mediterranean Sea alone. GTAs and viruses are efficient HGT vehicles with a major impact on prokaryotic evolution.

As a consequence of this modern DNA analysis, the idea that eukaryotes evolved directly from Archaea has fallen out of favor. While eukaryotes share many features that are absent in bacteria, such as the TATA box (located in many genes' promoter region), the discovery that some eukaryotic genes were more homologous with bacterial DNA than Archaea DNA made this idea less tenable. Furthermore, scientists have proposed genome fusion from Archaea and Bacteria by endosymbiosis as the ultimate event in eukaryotic evolution.

HGT in Eukaryotes

Although it is easy to see how prokaryotes exchange genetic material by HGT, scientists initially thought that this process was absent in eukaryotes. After all, prokaryotes are but single cells exposed directly to their environment whereas, the multicellular organisms' sex cells are usually sequestered in protected parts of the body. It follows from this idea that the gene transfers between multicellular eukaryotes should be more difficult. Scientists believe this process is rarer in eukaryotes and has a much smaller evolutionary impact than in prokaryotes. In spite of this, HGT between distantly related organisms is evident in several eukaryotic species, and it is possible that scientists will discover more examples in the future.

In plants, researchers have observed gene transfer in species that cannot cross-pollinate by normal means. Transposons or “jumping genes” have shown a transfer between rice and millet plant species. Furthermore, fungal species feeding on yew trees, from which the anti-cancer drug TAXOL® is derived from the bark, have acquired the ability to make taxol themselves, a clear example of gene transfer.

In animals, a particularly interesting example of HGT occurs within the aphid species (Figure 20.13). Aphids are insects that vary in color based on carotenoid content. Carotenoids are pigments that a variety of plants, fungi, and microbes produce, and they serve a variety of functions in animals, who obtain these chemicals from their food. Humans require carotenoids to synthesize vitamin A, and we obtain them by eating orange fruits and vegetables: carrots, apricots, mangoes, and sweet potatoes. Alternatively, aphids have acquired the ability to make the carotenoids on their own. According to DNA analysis, this ability is due to fungal genes transferring into the insect by HGT, presumably as the insect consumed fungi for food. A carotenoid enzyme, or desaturase, is responsible for the red coloration in certain aphids, and when mutation of this gene leads to formation of inactive enzyme, the aphids revert to their more common green color (Figure 20.13).

Genome Fusion and Eukaryote Evolution

Scientists believe the ultimate in HGT occurs through genome fusion between different prokaryote species when two symbiotic organisms become endosymbiotic. This occurs when one species is taken inside another species' cytoplasm, which ultimately results in a genome consisting of genes from both the endosymbiont and the host. This mechanism is an aspect of the Endosymbiont Theory, which most biologists accept as the mechanism whereby eukaryotic cells obtained their mitochondria and chloroplasts. However, the role of endosymbiosis in developing the nucleus is more controversial. Scientists believe that nuclear and mitochondrial DNA have different (separate) evolutionary origins, with the mitochondrial DNA being derived from the bacteria's circular genomes engulfed by ancient prokaryotic cells. We can regard mitochondrial DNA as the smallest chromosome. Interestingly enough, mitochondrial DNA is inherited only from the mother. The mitochondrial DNA degrades in sperm when the sperm degrades in the fertilized egg or in other instances when the mitochondria located in the sperm's flagellum fails to enter the egg.

Within the past decade, James Lake of the UCLA/NASA Astrobiology Institute proposed that the genome fusion process is responsible for the evolution of the first eukaryotic cells (Figure 20.14a). Using DNA analysis and a new mathematical algorithm, conditioned reconstruction (CR), his laboratory proposed that eukaryotic cells developed from an endosymbiotic gene fusion between two species, one an Archaea and the other a Bacteria. As mentioned, some eukaryotic genes resemble those of Archaea whereas, others resemble those from Bacteria. An endosymbiotic fusion event, such as Lake has proposed, would clearly explain this observation. Alternatively, this work is new and the CR algorithm is relatively unsubstantiated, which causes many scientists to resist this hypothesis.

Lake's more recent work (Figure 20.14b) proposes that gram-negative bacteria, which are unique within their domain in that they contain two lipid bilayer membranes, resulted from an endosymbiotic fusion of archaeal and bacterial species. The double membrane would be a direct result of the endosymbiosis, with the endosymbiont picking up the second membrane from the host as it was internalized. Scientists have also used this mechanism to explain the double membranes in mitochondria and chloroplasts. Some are skeptical of Lake’s work, and the biological science community still debates his ideas. In addition to Lake’s hypothesis, there are several other competing theories as to the origin of eukaryotes. How did the eukaryotic nucleus evolve? One theory is that the prokaryotic cells produced an additional membrane that surrounded the bacterial chromosome. Some bacteria have the DNA enclosed by two membranes however, there is no evidence of a nucleolus or nuclear pores. Other proteobacteria also have membrane-bound chromosomes. If the eukaryotic nucleus evolved this way, we would expect one of the two types of prokaryotes to be more closely related to eukaryotes.

The nucleus-first hypothesis proposes that the nucleus evolved in prokaryotes first (Figure 20.15a), followed by a later fusion of the new eukaryote with bacteria that became mitochondria. The mitochondria-first hypothesis proposes that mitochondria were first established in a prokaryotic host (Figure 20.15b), which subsequently acquired a nucleus, by fusion or other mechanisms, to become the first eukaryotic cell. Most interestingly, the eukaryote-first hypothesis proposes that prokaryotes actually evolved from eukaryotes by losing genes and complexity (Figure 20.15c). All of these hypotheses are testable. Only time and more experimentation will determine which hypothesis data best supports.

Web and Network Models

Recognizing the importance of HGT, especially in prokaryote evolution, has caused some to propose abandoning the classic “tree of life” model. In 1999, W. Ford Doolittle proposed a phylogenetic model that resembles a web or a network more than a tree. The hypothesis is that eukaryotes evolved not from a single prokaryotic ancestor, but from a pool of many species that were sharing genes by HGT mechanisms. As Figure 20.16a shows, some individual prokaryotes were responsible for transferring the bacteria that caused mitochondrial development to the new eukaryotes whereas, other species transferred the bacteria that gave rise to chloroplasts. Scientists often call this model the “ web of life .” In an effort to save the tree analogy, some have proposed using the Ficus tree (Figure 20.16b) with its multiple trunks as a phylogenetic way to represent a diminished evolutionary role for HGT.

Ring of Life Models

Others have proposed abandoning any tree-like model of phylogeny in favor of a ring structure, the so-called “ ring of life ” (Figure 20.17). This is a phylogenetic model where all three domains of life evolved from a pool of primitive prokaryotes. Lake, again using the conditioned reconstruction algorithm, proposes a ring-like model in which species of all three domains—Archaea, Bacteria, and Eukarya—evolved from a single pool of gene-swapping prokaryotes. His laboratory proposes that this structure is the best fit for data from extensive DNA analyses performed in his laboratory, and that the ring model is the only one that adequately takes HGT and genomic fusion into account. However, other phylogeneticists remain highly skeptical of this model.

In summary, we must modify Darwin's “tree of life” model to include HGT. Does this mean abandoning the tree model completely? Even Lake argues that scientists should attempt to modify the tree model to allow it to accurately fit his data, and only the inability to do so will sway people toward his ring proposal.

This doesn’t mean a tree, web, or a ring will correlate completely to an accurate description of phylogenetic relationships of life. A consequence of the new thinking about phylogenetic models is the idea that Darwin’s original phylogenetic tree concept is too simple, but made sense based on what scientists knew at the time. However, the search for a more useful model moves on: each model serves as hypotheses to test with the possibility of developing new models. This is how science advances. Researchers use these models as visualizations to help construct hypothetical evolutionary relationships and understand the massive amount of data that requires analysis.


20.3 Perspectives on the Phylogenetic Tree

In this section, you will explore the following questions:

  • What is horizontal gene transfer and its significance in constructing phylogenetic trees?
  • How do prokaryotes and eukaryotes transfer genes horizontally?
  • What are other models of phylogenetic relationships and how do they differ from the original phylogenetic tree concept?

Connection for AP ® Courses

Newer technologies have uncovered surprising discoveries with unexpected relationships among organisms, such as the fact that humans seems to be more closely related to fungi than fungi are to plants. (Think about that the next time you see a mushroom). As the information about DNA sequences grows, scientists will become closer to mapping a more accurate evolutionary history of all life on Earth.

What makes phylogeny difficult, especially among prokaryotes, is the transfer of genes horizontally (horizontal gene transfer, or HGT) between unrelated species. Like mutations, HGT introduces genetic variation into the bacterial population. This passing of genes between species adds a layer of complexity to understanding relatedness.

Information presented and the examples highlighted in the section support concepts outlined in Big Idea 3 of the AP ® Biology Curriculum Framework. The AP ® Learning Objectives listed in the Curriculum Framework provide a transparent foundation for the AP ® Biology course, an inquiry-based laboratory experience, instructional activities, and AP ® exam questions. A learning objective merges required content with one or more of the seven science practices.

Big Idea 1 The process of evolution drives the diversity and unity of life.
Enduring Understanding 1.B Organisms are linked by lines of descent from common ancestry.
Essential Knowledge 1.B.1 Organisms share many conserved core processes and features that evolved and are widely distributed among organisms today.
Science Practice 3.1 The student can pose scientific questions.
Learning Objective 1.14 The student is able to pose scientific questions that correctly identify essential properties of shared, core life processes that provide insight into the history of life on Earth.
Essential Knowledge 1.B.1 Organisms share many conserved core processes and features that evolved and are widely distributed among organisms today.
Science Practice 7.2 The student can connect concepts in and across domain(s) to generalize or extrapolate in and/or across enduring understandings and/or big ideas.
Learning Objective 1.15 The student is able to describe specific examples of conserved core biological processes and features shared by all domains or within one domain of life, and how these shared, conserved core processes and features support the concept of common ancestry for all organisms.
Big Idea 3 Living systems store, retrieve, transmit and respond to information essential to life processes.
Enduring Understanding 3.C The processing of genetic information is imperfect and is a source of genetic variation.
Essential Knowledge 3.C.2 Biological systems have multiple processes that increase genetic variation.
Science Practice 6.2 The student can construct explanations of phenomena based on evidence produced through scientific practices.
Learning Objective 3.27 The student is able to construct an explanation of processes that increase variation within a population.

The concepts of phylogenetic modeling are constantly changing. It is one of the most dynamic fields of study in all of biology. Over the last several decades, new research has challenged scientists’ ideas about how organisms are related. New models of these relationships have been proposed for consideration by the scientific community.

Many phylogenetic trees have been shown as models of the evolutionary relationship among species. Phylogenetic trees originated with Charles Darwin, who sketched the first phylogenetic tree in 1837 (Figure 20.12a), which served as a pattern for subsequent studies for more than a century. he phylogenetic tree concept with a single trunk representing a shared ancestry, with the branches representing the divergence of species from this ancestry, fits well with the structure of many common trees, such as the oak (Figure 20.12b). However, evidence from modern DNA sequence analysis and newly developed computer algorithms has caused skepticism about the validity of the standard tree model in the scientific community.

Limitations to the Classic Model

Classical thinking about prokaryotic evolution, included in the classic tree model, is that species evolve clonally. That is, they produce offspring themselves with only random mutations causing the descent into the variety of modern-day and extinct species known to science. This view is somewhat complicated in eukaryotes that reproduce sexually, but the laws of Mendelian genetics explain the variation in offspring, again, to be a result of a mutation within the species. The concept of genes being transferred between unrelated species was not considered as a possibility until relatively recently. Horizontal gene transfer (HGT), also known as lateral gene transfer, is the transfer of genes between unrelated species. HGT has been shown to be an ever-present phenomenon, with many evolutionists postulating a major role for this process in evolution, thus complicating the simple tree model. Genes have been shown to be passed between species which are only distantly related using standard phylogeny, thus adding a layer of complexity to the understanding of phylogenetic relationships.

The various ways that HGT occurs in prokaryotes is important to understanding phylogenies. Although at present HGT is not viewed as important to eukaryotic evolution, HGT does occur in this domain as well. Finally, as an example of the ultimate gene transfer, theories of genome fusion between symbiotic or endosymbiotic organisms have been proposed to explain an event of great importance—the evolution of the first eukaryotic cell, without which humans could not have come into existence.

Horizontal Gene Transfer

Horizontal gene transfer (HGT) is the introduction of genetic material from one species to another species by mechanisms other than the vertical transmission from parent(s) to offspring. These transfers allow even distantly related species to share genes, influencing their phenotypes. It is thought that HGT is more prevalent in prokaryotes, but that only about 2% of the prokaryotic genome may be transferred by this process. Some researchers believe such estimates are premature: the actual importance of HGT to evolutionary processes must be viewed as a work in progress. As the phenomenon is investigated more thoroughly, it may be revealed to be more common. Many scientists believe that HGT and mutation appear to be (especially in prokaryotes) a significant source of genetic variation, which is the raw material for the process of natural selection. These transfers may occur between any two species that share an intimate relationship (Table 20.1).

Mechanism Mode of Transmission Example
Prokaryotes transformation DNA uptake many prokaryotes
transduction bacteriophage (virus) bacteria
conjugation pilus many prokaryotes
gene transfer agents phage-like particles purple non-sulfur bacteria
Eukaryotes from food organisms unknown aphid
jumping genes transposons rice and millet plants
epiphytes/parasites unknown yew tree fungi
from viral infections

HGT in Prokaryotes

The mechanism of HGT has been shown to be quite common in the prokaryotic domains of Bacteria and Archaea, significantly changing the way their evolution is viewed. The majority of evolutionary models, such as in the Endosymbiont Theory, propose that eukaryotes descended from multiple prokaryotes, which makes HGT all the more important to understanding the phylogenetic relationships of all extant and extinct species.

The fact that genes are transferred among common bacteria is well known to microbiology students. These gene transfers between species are the major mechanism whereby bacteria acquire resistance to antibiotics. Classically, this type of transfer has been thought to occur by three different mechanisms:

  1. Transformation: naked DNA is taken up by a bacteria
  2. Transduction: genes are transferred using a virus
  3. Conjugation: the use a hollow tube called a pilus to transfer genes between organisms

More recently, a fourth mechanism of gene transfer between prokaryotes has been discovered. Small, virus-like particles called gene transfer agents (GTAs) transfer random genomic segments from one species of prokaryote to another. GTAs have been shown to be responsible for genetic changes, sometimes at a very high frequency compared to other evolutionary processes. The first GTA was characterized in 1974 using purple, non-sulfur bacteria. These GTAs, which are thought to be bacteriophages that lost the ability to reproduce on their own, carry random pieces of DNA from one organism to another. The ability of GTAs to act with high frequency has been demonstrated in controlled studies using marine bacteria. Gene transfer events in marine prokaryotes, either by GTAs or by viruses, have been estimated to be as high as 10 13 per year in the Mediterranean Sea alone. GTAs and viruses are thought to be efficient HGT vehicles with a major impact on prokaryotic evolution.

As a consequence of this modern DNA analysis, the idea that eukaryotes evolved directly from Archaea has fallen out of favor. While eukaryotes share many features that are absent in bacteria, such as the TATA box (found in the promoter region of many genes), the discovery that some eukaryotic genes were more homologous with bacterial DNA than Archaea DNA made this idea less tenable. Furthermore, the fusion of genomes from Archaea and Bacteria by endosymbiosis has been proposed as the ultimate event in eukaryotic evolution.

HGT in Eukaryotes

Although it is easy to see how prokaryotes exchange genetic material by HGT, it was initially thought that this process was absent in eukaryotes. After all, prokaryotes are but single cells exposed directly to their environment, whereas the sex cells of multicellular organisms are usually sequestered in protected parts of the body. It follows from this idea that the gene transfers between multicellular eukaryotes should be more difficult. Indeed, it is thought that this process is rarer in eukaryotes and has a much smaller evolutionary impact than in prokaryotes. In spite of this fact, HGT between distantly related organisms has been demonstrated in several eukaryotic species, and it is possible that more examples will be discovered in the future.

In plants, gene transfer has been observed in species that cannot cross-pollinate by normal means. Transposons or “jumping genes” have been shown to transfer between rice and millet plant species. Furthermore, fungal species feeding on yew trees, from which the anti-cancer drug paclitaxel is derived from the bark, have acquired the ability to make paclitaxel themselves, a clear example of gene transfer.

In animals, a particularly interesting example of HGT occurs within the aphid species (Figure 20.13). Aphids are insects that vary in color based on carotenoid content. Carotenoids are pigments made by a variety of plants, fungi, and microbes, and they serve a variety of functions in animals, who obtain these chemicals from their food. Humans require carotenoids to synthesize vitamin A, and we obtain them by eating orange fruits and vegetables: carrots, apricots, mangoes, and sweet potatoes. On the other hand, aphids have acquired the ability to make the carotenoids on their own. According to DNA analysis, this ability is due to the transfer of fungal genes into the insect by HGT, presumably as the insect consumed fungi for food. A carotenoid enzyme called a desaturase is responsible for the red coloration seen in certain aphids, and it has been further shown that when this gene is mutated and the enzyme looses activity, the aphids revert back to their more common green color (Figure 20.13).

Everyday Connection for AP® Courses

Barbara McClintock (1902–1992) discovered transposons while working on maize genetics.

  1. that mitochondria were first established in a prokaryotic host which acquired a nucleus to become the first eukaryotic cell
  2. that the nucleus evolved in prokaryotes first followed by fusion of the new eukaryote with bacteria that became mitochondria
  3. that prokaryotes actually evolved from eukaryotes by losing genes and complexity
  4. that eukaryotes developed Golgi before mitochondria

Genome Fusion and the Evolution of Eukaryotes

Scientists believe the ultimate in HGT occurs through genome fusion between different species of prokaryotes when two symbiotic organisms become endosymbiotic. This occurs when one species is taken inside the cytoplasm of another species, which ultimately results in a genome consisting of genes from both the endosymbiont and the host. This mechanism is an aspect of the Endosymbiont Theory, which is accepted by a majority of biologists as the mechanism whereby eukaryotic cells obtained their mitochondria and chloroplasts. However, the role of endosymbiosis in the development of the nucleus is more controversial. Nuclear and mitochondrial DNA are thought to be of different (separate) evolutionary origin, with the mitochondrial DNA being derived from the circular genomes of bacteria that were engulfed by ancient prokaryotic cells. Mitochondrial DNA can be regarded as the smallest chromosome. Interestingly enough, mitochondrial DNA is inherited only from the mother. The mitochondrial DNA degrades in sperm when the sperm degrades in the fertilized egg or in other instances when the mitochondria located in the flagellum of the sperm fails to enter the egg.

Within the past decade, the process of genome fusion by endosymbiosis has been proposed by James Lake of the UCLA/NASA Astrobiology Institute to be responsible for the evolution of the first eukaryotic cells (Figure 20.15a). Using DNA analysis and a new mathematical algorithm called conditioned reconstruction (CR), his laboratory proposed that eukaryotic cells developed from an endosymbiotic gene fusion between two species, one an Archaea and the other a Bacteria. As mentioned, some eukaryotic genes resemble those of Archaea, whereas others resemble those from Bacteria. An endosymbiotic fusion event, such as Lake has proposed, would clearly explain this observation. On the other hand, this work is new and the CR algorithm is relatively unsubstantiated, which causes many scientists to resist this hypothesis.

More recent work by Lake (Figure 20.15b) proposes that gram-negative bacteria, which are unique within their domain in that they contain two lipid bilayer membranes, indeed resulted from an endosymbiotic fusion of archaeal and bacterial species. The double membrane would be a direct result of the endosymbiosis, with the endosymbiont picking up the second membrane from the host as it was internalized. This mechanism has also been used to explain the double membranes found in mitochondria and chloroplasts. Some are skeptical of Lake’s work, and the biological science community still debates his ideas. In addition to Lake’s hypothesis, there are several other competing theories as to the origin of eukaryotes. How did the eukaryotic nucleus evolve? One theory is that the prokaryotic cells produced an additional membrane that surrounded the bacterial chromosome. Some bacteria have the DNA enclosed by two membranes however, there is no evidence of a nucleolus or nuclear pores. Other proteobacteria also have membrane-bound chromosomes. If the eukaryotic nucleus evolved this way, we would expect one of the two types of prokaryotes to be more closely related to eukaryotes.

The nucleus-first hypothesis proposes that the nucleus evolved in prokaryotes first (Figure 20.16a), followed by a later fusion of the new eukaryote with bacteria that became mitochondria. The mitochondria-first hypothesis proposes that mitochondria were first established in a prokaryotic host (Figure 20.16b), which subsequently acquired a nucleus, by fusion or other mechanisms, to become the first eukaryotic cell. Most interestingly, the eukaryote-first hypothesis proposes that prokaryotes actually evolved from eukaryotes by losing genes and complexity (Figure 20.16c). All of these hypotheses are testable. Only time and more experimentation will determine which hypothesis is best supported by data.

Web and Network Models

The recognition of the importance of HGT, especially in the evolution of prokaryotes, has caused some to propose abandoning the classic “tree of life” model. In 1999, W. Ford Doolittle proposed a phylogenetic model that resembles a web or a network more than a tree. The hypothesis is that eukaryotes evolved not from a single prokaryotic ancestor, but from a pool of many species that were sharing genes by HGT mechanisms. As shown in Figure 20.17a, some individual prokaryotes were responsible for transferring the bacteria that caused mitochondrial development to the new eukaryotes, whereas other species transferred the bacteria that gave rise to chloroplasts. This model is often called the “web of life.” In an effort to save the tree analogy, some have proposed using the Ficus tree (Figure 20.17b) with its multiple trunks as a phylogenetic to represent a diminished evolutionary role for HGT.

Ring of Life Models

Others have proposed abandoning any tree-like model of phylogeny in favor of a ring structure, the so-called “ring of life” (Figure 20.18) a phylogenetic model where all three domains of life evolved from a pool of primitive prokaryotes. Lake, again using the conditioned reconstruction algorithm, proposes a ring-like model in which species of all three domains—Archaea, Bacteria, and Eukarya—evolved from a single pool of gene-swapping prokaryotes. His laboratory proposes that this structure is the best fit for data from extensive DNA analyses performed in his laboratory, and that the ring model is the only one that adequately takes HGT and genomic fusion into account. However, other phylogeneticists remain highly skeptical of this model.

In summary, the “tree of life” model proposed by Darwin must be modified to include HGT. Does this mean abandoning the tree model completely? Even Lake argues that all attempts should be made to discover some modification of the tree model to allow it to accurately fit his data, and only the inability to do so will sway people toward his ring proposal.

This doesn’t mean a tree, web, or a ring will correlate completely to an accurate description of phylogenetic relationships of life. A consequence of the new thinking about phylogenetic models is the idea that Darwin’s original conception of the phylogenetic tree is too simple, but made sense based on what was known at the time. However, the search for a more useful model moves on: each model serving as hypotheses to be tested with the possibility of developing new models. This is how science advances. These models are used as visualizations to help construct hypothetical evolutionary relationships and understand the massive amount of data being analyzed.

The transfer of genes by a mechanism not involving asexual reproduction is called:

Particles that transfer genetic material from one species to another, especially in marine prokaryotes:

What does the trunk of the classic phylogenetic tree represent?

Which phylogenetic model proposes that all three domains of life evolved from a pool of primitive prokaryotes?

Compare three different ways that eukaryotic cells may have evolved.

Some hypotheses propose that mitochondria were acquired first, followed by the development of the nucleus. Others propose that the nucleus evolved first and that this new eukaryotic cell later acquired the mitochondria. Still others hypothesize that prokaryotes descended from eukaryotes by the loss of genes and complexity.

Describe how aphids acquired the ability to change color.

Aphids have acquired the ability to make the carotenoids on their own. DNA analysis has demonstrated that this ability is due to the transfer of fungal genes into the insect by HGT, presumably as the insect consumed fungi for food.

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    Hand-washing resistant bacteria. Will they evolve one day? - Biology

    by
    Jason Dulle
    [email protected]

    Years ago I was discussing evolution with a co-worker. I asked her if she thought evolution was true. She heartily replied, &ldquoYes, I do.&rdquo When I asked, &ldquoWhy do you think it is true?&rdquo, she responded, &ldquoI&rsquoll have to get back to you on that.&rdquo While her honesty was atypical, her posture was not. Many people accept Darwin&rsquos theory of evolution without a sufficient understanding of the theory, and without sufficient evidence. As Michael Behe once quipped, most people&rsquos knowledge of evolution extends little beyond that of the car decal depicting a fish with feet. 1

    In my experience, the reason most people accept Darwin&rsquos theory is because it is the scientific consensus. They reason that scientists base their claims on the evidence, so if most scientists believe in evolution, it follows that the evidence for evolution must be compelling. What they fail to understand is that scientists, like everyone else, bring certain biases and philosophical perspectives to the evidence. Like the proverbial tail that wags the dog, sometimes their conclusions are driven more by their philosophical assumptions than by the empirical evidence itself. Such is the case when it comes to Darwinian evolution. While experimental evidence has demonstrated that natural selection working on random mutation can account for trivial changes within species ­­&ndash such as the size of finch beaks and antibiotic resistance in bacteria ­&ndash there is no evidence that Darwin&rsquos mechanism is sufficient to create new biological information and novel biological systems, and hence it cannot account for the proliferation of species as Darwin suggested. Indeed, recent experimental evidence disconfirms the notion.

    What Needs to be Explained

    To properly evaluate Darwin&rsquos theory of the evolution of life we must first clarify what is meant by &ldquoevolution.&rdquo In its most basic sense evolution refers to small biological changes within a species over time. Called &ldquomicroevolution,&rdquo or the special theory of evolution, this definition of evolution is relatively uncontroversial and has been empirically confirmed (e.g. drug resistance in bacteria, changes in the size of finch beaks, etc.). Evolution can also refer to large-scale biological changes 2 that, over time, transform one species into another into another ad infinitum. This kind of evolution is called macroevolution, or the general theory of evolution. Darwin&rsquos theory entails this latter definition, and thus proof for his theory requires evidence that there are no natural limits to the amount of biological variation an organism can undergo.

    Have Darwinists met their burden of proof? No. To date, no evidence for macroevolution has been provided. Darwinists routinely offer the evidence for microevolution as if that is evidence for macroevolution, but this is a methodologically illegitimate extrapolation from the evidence. Evidence for microevolution is just that: evidence for microevolution. It is not, in itself, evidence for macroevolution. To be sure, the reality of microevolution makes macroevolution a plausible concept because it proves organisms are capable of experiencing biological change of some sort, but more than plausibility is required if we are to take Darwinism seriously. Minimally, Darwinists need to offer (1) empirical proof that there are no natural limits to genetic change, (2) a detailed biological pathway for the transition from one organism to another, as well as (3) evidence that this pathway could reasonably be traversed given the amount of time available. Without such a demonstration, there is no reason to think macroevolution is anything more than an unsubstantiated hypothesis.

    What does the evidence reveal? It strongly suggests there is a natural limit to the amount of variation organisms can undergo before they reach an evolutionary ceiling. As Gilbert, Opitz, and Raff wrote:

    The Modern Synthesis is a remarkable achievement. However, starting in the 1970s, many biologists began questioning its adequacy in explaining evolution. Genetics might be adequate for explaining microevolution, but microevolutionary changes in gene frequency were not seen as able to turn a reptile into a mammal or to convert a fish into an amphibian. Microevolution looks at adaptations that concern only the survival of the fittest, not the arrival of the fittest. As Goodwin (1995) points out, &ldquothe origin of species&mdashDarwin's problem&mdashremains unsolved.&rdquo 3

    Everything we know about organisms tells us they are more like balloons than Play-doh: They are capable of experiencing a range of change, but only within prescribed limits. It would be foolish to assume that because we can inflate a balloon to the size of a basketball, given enough time it could be inflated to the size of a planet. Likewise, it is foolish to think that just because an organism is capable of undergoing small biological changes, given enough time it will become an entirely different organism altogether. Balloons and DNA are designed with a measure of elasticity, but both have a breaking point beyond which no further change is possible. While beak sizes may change within a population of finches during seasons of drought, there is no empirical evidence demonstrating that finches can evolve into squirrels given enough time. The genetic evidence is overwhelmingly in favor of the conclusion that there are natural limits to genetic variability. And if there are natural limits to genetic variability, Darwinism is proven false.

    The Origin of Biological Information

    If macroevolution occurs in biological systems, it must do so at the biochemical level. Additional genomic information is needed to build the new proteins and biological systems required for large-scale changes. Where does the new biological information come from? Mutations? No. Point mutations, such as insertions, inversions, or substitutions of nucleotides in existing genes cannot increase the information content of DNA even if they occur in protein-coding regions, and even if the mutations are beneficial to the organism. At best they can only replace existing information/function with different information/function, so that the overall information content is preserved. 4 Macroevolution requires a net increase of biological information, not just a change in existing information.

    The origination of new genetic information requires new proteins, each of which requires hundreds of additional nucleotides arranged in a highly specified order. How likely is it that chance processes can get the job done? Next to none! The chances of producing a functional amino acid sequence of a mere 150 nucleotide bases (which would sequence one of the smallest proteins) is 1 in 10 164 . 5 To put this number in perspective, consider that there have only been 10 139 events in the entire universe since the Big Bang. 6 Even if every event in the history of the universe was devoted to building a single functional protein, the number of sequences produced thus far would be less than 1 out of a trillion trillion of the total number of events needed to give it even a 50% chance of success! A reasonable person must conclude, then, that it is beyond the reach of chance to create even the smallest amount of new biological information in an organism. Add to this the fact that many new proteins are needed to produce new biological systems, and the scenario becomes all the more fantastical. If chance alone cannot produce the gene for even one protein&mdashyet alone many&mdashmacroevolution becomes impossible.

    While single point mutations cannot get the job done, what about whole gene duplication (when a gene is copied twice, thus becoming two identical genes)? Can this account for new biological information? No. The reason is simple: Duplicating a gene does not increase the net information content of the cell, but merely repeats existing information. There is another reason for thinking gene duplication cannot account for new biological information: Duplicating a gene does not increase the net information content of the cell, but merely repeats existing information. Do you want more proof? Here&rsquos a third reason: Duplicating a gene does not increase the net information content of the cell, but merely repeats existing information.

    Surely you just said to yourself, &ldquoThat&rsquos not three reasons, but one. You simply repeated yourself three times.&rdquo Exactly! That&rsquos the point. Duplicating existing information cannot produce new information. Just as saying, &ldquoduplicating a gene does not increase the net information content of the cell&rdquo three times does not triple the information content of the sentence, duplicating a gene cannot increase the information content of the cell. Gene duplication cannot help an organism perform some new function. Trying to get new biological information/function by duplicating an existing gene is like thinking you can obtain an engine for your car by making a second steering wheel!

    Gene Duplication + Point Mutations

    While neither gene duplication nor point mutations can independently increase the information content of DNA, could they do so together? Some suggest that new information could be gained by gene duplication followed by numerous single point mutations over a long period of time, so that eventually the duplicated gene spells out a different biological message than the original.

    There are some examples in which it is likely that gene duplication followed by point mutations has resulted in a functional gene that differs from the parent gene: e.g. the two gamma-globin coding regions on human chromosome 11. The second gamma-globin gene probably resulted from a duplication of a single gamma-globin gene, followed by a single point mutation. It should be noted, however, that only one codon experienced change, no new biological systems were produced, and the function of the second gamma-globin gene differs little from its parent. 7 While this is an important biological change, it is impotent to advance macroevolutionary change.

    If we are to believe gene duplication followed by point mutations is capable of producing the raw materials for genuine biological innovation, minimally we need to know if the cell is capable of producing enough duplicated genes. Douglas Futuyma estimates that the gene duplication rate is &ldquoabout 0.01 duplication[s] per gene per million years.&rdquo 8 That means it would take 100 million year to duplicate any given gene. If an organism requires multiple copies of the same gene to produce an adaptable change, its evolution will be extremely slow. For example, the Antarctic eelpout fish required 30 copies of an anti-freeze gene to survive the icy waters of the Antarctic Ocean. According to evolutionists the Antarctic eelpout would have had to have experienced all 30 duplications in a period of less than 50 million years. And yet given Futuyma&rsquos calculations, we could only expect that many duplications after 3 billion years!

    The real question is whether gene duplication followed by point mutations is capable of increasing the biological information of an organism and creating new biological systems. There are numerous reasons to think the answer to these questions is a resounding no. It is highly unlikely that all point mutations will be beneficial. Consider something as simple as HTML code. If one randomly inserts, inverts, and deletes various characters in the code, what are the chances that every change will be beneficial? The chances are extremely low. The chances are overwhelmingly greater that most changes will be deleterious to the integrity and function of the code. Likewise, as soon as one or more harmful mutations accumulate in a critical region of the gene, the gene will either cease to function or function sub-optimally, affecting the organism&rsquos fitness. And because energy is required to preserve this broken gene in subsequent generations, the organism&rsquos overall fitness will decrease.

    But what if &ndash by chance &ndash every mutation was a beneficial one? Over time, couldn&rsquot the gene evolve to form new genetic information? Apart from the extremely unlikely possibility that the duplicate gene would experience beneficial &ndash and only beneficial mutations &ndash is it reasonable to think new genetic information could be gained through such a process? No, because the gene would need to remain functional throughout the evolutionary process (i.e. it must always convey a biologically functional message) if it is to provide a survival advantage to the organism nature can select for. How could this be done by changing one nucleotide at a time? While small amounts of information could conceivably maintain function while undergoing slight, successive evolutionary changes, it is inconceivable that the same could happen for large amounts of biological information. For example, we could evolve WORD into GENE one letter at a time and preserve meaning throughout the process:

    WORD
    WORE
    GORE
    GONE
    GENE

    But what if we had to evolve &ldquogene duplication does not provide additional genetic information&rdquo into &ldquowe have to consider the fact that double point mutations are highly improbable&rdquo one letter at a time? How could the sentence retain meaning at every step of the evolutionary process? It is impossible, and my analogy only contains 66 characters. Most genes contain hundreds of genetic characters (nucleotides)! And yet for macroevolution to occur, this process would need to repeat itself millions of times over.

    On a purely conceptual level alone, it seems inconceivable that random mutations could be responsible for macroevolutionary changes in organisms. Ultimately, however, it is the empirical data that must decide the matter. Joseph Bozorgmeh summarizes the empirical data in the abstract of his paper &ldquoIs gene duplication a viable explanation for the origination of biological information and complexity?&rdquo:

    All life depends on the biological information encoded in DNA with which to synthesize and regulate various peptide sequences required by an organism's cells. Hence, an evolutionary model accounting for the diversity of life needs to demonstrate how novel exonic regions that code for distinctly different functions can emerge. Natural selection tends to conserve the basic functionality, sequence, and size of genes and, although beneficial and adaptive changes are possible, these serve only to improve or adjust the existing type. However, gene duplication allows for a respite in selection and so can provide a molecular substrate for the development of biochemical innovation. Reference is made here to several well-known examples of gene duplication, and the major means of resulting evolutionary divergence, to examine the plausibility of this assumption. The totality of the evidence reveals that, although duplication can and does facilitate important adaptations by tinkering with existing compounds, molecular evolution is nonetheless constrained in each and every case. Therefore, although the process of gene duplication and subsequent random mutation has certainly contributed to the size and diversity of the genome, it is alone insufficient in explaining the origination of the highly complex information pertinent to the essential functioning of living organisms. 9

    In the body of the paper he writes:

    The various postduplication mechanisms entailing random mutations and recombinations considered were observed to tweak, tinker, copy, cut, divide, and shuffle existing genetic information around, but fell short of generating genuinely distinct and entirely novel functionality. Contrary to Darwin&rsquos view of the plasticity of biological features, successive modification and selection in genes does indeed appear to have real and inherent limits: it can serve to alter the sequence, size, and function of a gene to an extent, but this almost always amounts to a variation on the same theme&mdashas with RNASE1B in colobine monkeys. The conservation of all-important motifs within gene families, such as the homeobox or the MADS-box motif, attests to the fact that gene duplication results in the copying and preservation of biological information, and not its transformation as something original. 10

    Having determined that gene duplication cannot account for biological novelty, we now turn our attention to what scientific research has revealed about the power of random mutation to create biological novelties. How much biological change can it account for?

    The Creative Power of Mutations Tested and Found Wanting

    The heart of the neo-Darwinian synthesis is that evolution advances via the process of natural selection working on random mutations (RM+NS). Natural selection itself lacks any creative power &ndash it only eliminates what doesn&rsquot work. Eliminating the unfit, however, does nothing to &ldquoexplain the origin of the fit&rdquo! 11 The burden falls entirely on RM to create the biological novelties required by Darwinism to drive evolution forward. It must be asked, then, whether RM has the creative power required by Darwin&rsquos theory. Can RM produce the new biological information necessary to drive evolution forward and explain the diversification of all life? What exactly can RM do? Michael Behe evaluated these question in-depth in his book, The Edge of Evolution. Much of wat follows is a summary of Behe&rsquos argument.

    When the neo-Darwinian synthesis was set forth some 70 years ago, answers to these questions could not be ascertained. While the theory was plausible on a conceptual level, there was no way of testing it directly on an empirical level. Over the last 30 years, however, we have been able to observe both the power and limits of RM+NS at the biological level, and are now in a good position to evaluate the power of RM+NS. What have we discovered? We discovered that while RM can produce variability within an organism, it is not capable of producing the kind of changes required by Darwin&rsquos theory. RM is severely limited in what it can accomplish.

    A Lack of Building Materials

    If we are to believe the process of natural selection working on random mutations is capable of creating novel biological information and structures, at least two conditions must be demonstrated empirically: (1) The mutation rate must be such that we can expect the raw materials necessary to create the novel biological information and structures required for macroevolution to both arise and become fixed in a given population within the time limits required for its evolution (2) The fitness gains provided by each beneficial mutation must be cumulative.

    Demonstrating the first condition has long been a challenge to Darwinism. In most organisms the mutation rate is 1 nucleotide per 100,000,000, and only a miniscule fraction of these mutations are ever beneficial to an organism. If, say, an organism requires 10,000 beneficial mutations over a period of 10 million years to evolve from species A into species B, and yet given the population size and mutation rate only 120 beneficial mutations can be expected to become fixed in the population during that time, then it would be impossible for that organism to experience macroevolution. The problem is analogous to building a brick house. If one is tasked with building a brick house in 30 days and the job requires 10,000 bricks, but the builder is only provided with two bricks per day, the home cannot be built in the time allotted. Such is the situation Darwinists find themselves in. The changes required for macroevolution are enormous, but the raw materials are few because beneficial mutations are so rare.

    As for the second condition, Darwinists have long assumed that fitness gains add up, so the more beneficial mutations the better! Recent experimental work by Rafael Sanjuán, Andrés Moya, and Santiago F. Elena, however, have undermined this assumption. Sanjuán et al found that when multiple beneficial mutations occur within an organism 12 , fitness is not improved but diminished. In their experiment, rather than working together (synergistic), beneficial mutations were observed to work against one another (antagonistic): &ldquo[A]ntagonistic epistasis represents the most abundant type of interaction among beneficial mutations, with several cases showing decompensatory epistasis.&rdquo They describe the importance of this finding as follows:

    [W]hen epistasis is decompensatory, both beneficial alleles involved in the interaction cannot spread to fixation in the population, because the double mutant is less fit than each single mutant. As a consequence, lineages bearing alternative beneficial mutations should compete with each other on their way to fixation and, as a consequence of asexuality and clonal interference, only the best competitor will eventually become fixed in the population. 13

    This puts Darwinists in a tough spot. When appearing alone, there are not enough beneficial mutations necessary for macroevolution. When multiple beneficial mutations arise simultaneously, they fight against one another and decrease the fitness of the organism. Either way, macroevolution is not possible.

    Many biological features require multiple mutations before any adaptive benefit can be conferred on the organism. Chemical engineer, Douglas Axe, published a paper in BIO-Complexity that sought to determine mathematically how long it would take for such a sequential combination of mutations to arise and become fixed in a population. To be generous to the Darwinist paradigm, Dr. Axe calculated the odds using asexual organisms. What did Axe discover? Assuming a constant population size of 1,000,000,000 organisms that reproduce three times per day every day for billions of years, up to six neutral mutations could become fixed in the population over the course of nearly four billion years (which is longer than the entire history of life on Earth). If the mutations were maladaptive (negative), then only two mutations could become fixed in a population over the same period of time.

    What does this mean? Put simply, there is not enough time to generate the number of mutations necessary to confer even minimally-complex adaptive advantages in microorganisms. When you consider the fact that the population size, reproduction rate, and years in existence of most organisms are orders of magnitude smaller than asexual microorganisms, the chances of such mutations arising in complex, multicellular populations is effectively zero. As Axe concludes:

    [T]he most significant implication comes not from how the two cases contrast but rather how they cohere―both showing severe limi tations to complex adaptation. To appreciate this, consider the tremendous number of cells needed to achieve adaptations of such limited complexity. As a basis for calculation, we have assumed a bacterial population that maintained an effective size of 10 9 individuals through 10 3 generations each year for billions of years. This amounts to well over a billion trillion opportunities (in the form of individuals whose lines were not destined to expire imminently) for evolutionary experimentation. Yet what these enormous resources are expected to have acc omplished, in terms of combined base changes, can be counted on the fingers. 14

    The best way to gauge the power of RM is by observing microbial life such as bacteria, parasites, and viruses because their populations are so numerous and their generation times so short. When it comes to evolvability, the most important factors are mutation rates, population sizes, and reproduction rates, not time. At an optimal reproduction rate of 30 minutes, a single E. coli bacterium can generate a population size of more than seven quadrillion organisms (7,000,000,000,000,000) in just 24 hours. Over the course of one year it can spawn 17,520 generations 15 . That&rsquos a lot of room for evolutionary advancement! Mammals cannot come close to such astronomical population sizes and generations, and thus we can learn what RM can do in mammals over a long period of time by observing what it can do in microbial life over a relatively short period of time (&ldquoshort&rdquo from a mammalian perspective).

    Richard Lenski has been culturing E. coli for more than 50,000 generations, which is equivalent to approximately 1,000,000 years of human evolution. 16 What has RM been observed to produce? Nothing much. No new genes, biological information, or biological systems have developed. According the Lenski, &ldquothe most profound change&rdquo he has observed is the ability some E. coli evolved to digest citrate. While this is a bona fide positive change, it is not all that remarkable when you consider the following:

    1. E. coli can normally digest citrate in anaerobic (absence of oxygen) conditions.
    2. The E. coli already possessed the enzymes necessary to metabolize citrate. They only lacked a way of getting citrate through their membrane in the presence of oxygen. 17 The situation is analogous to a fox living on a chicken farm. While he possesses the ability to digest those chickens, he does not do so because he is separated from them by an impenetrable fence. Once that fence is breached, however, that fox can and will eat his heart out!
    3. It took 32,000 generations to produce this tiny change. At this rate of evolutionary improvement, it would take billions of years for complex organisms like mammals to change from one species to another (since our population sizes and reproduction rates are orders of magnitude smaller than bacteria), but Darwinism requires that it happen in 10s, 100s, or 1000s of years.
    4. Why should it take so long for E. coli to develop this transport mechanism, when they&rsquove been swimming in citrate for so long?
    5. If E. coli could only evolve one major biological improvement in the equivalent of

    All of the observed changes in Lenski&rsquos E. coli are examples of microevolution, not macroevolution. The population began as E. coli,and millions of mutations and thousands of generations later, they remain E. coli. In fact, rather than gaining complexity and fitness, some of the E. coli populations have been observed to be in a state of devolution. Some have lost their ability to repair DNA during transcription, resulting in a mutation rate that is 70 times that of normal E. coli. As a result, they are losing genetic information, not gaining it devolving, not evolving. 18

    Dr. Ann Gauger, developmental biologist and senior research scientist at the Biologic Institute, co-authored a paper with Ralph Seelke in BIO-Complexity (&ldquoReductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness,&rdquo Vol. 2010) reporting on a laboratory experiment which demonstrates that evolutionary adaptation usually results from eliminating genetic information/machinery rather than building new genetic information/machinery. Dr. Gauger described her research as follows:

    When challenged to grow in medium with very little tryptophan, 14 different populations of cells reduced or eliminated genes for making tryptophan, rather than fixing the broken tryptophan-making gene they carried. (Fixing the gene would have required cells to revert two specific mutations, with each reversion itself conferring a growth advantage.) Because reducing or eliminating expression of the broken gene was &ldquoadaptive,&rdquo i.e. it allowed them to reproduce faster than cells still expressing the broken gene, and because there are many more ways to reduce or eliminate gene expression than to fix the gene, the populations always chose to reduce or eliminate gene function. 19

    Joseph Bozorgmehr also notes that &ldquo[i]n many instances. a loss of function and regulation in a harsh or unusual environment can have a beneficial outcome and thus be selected for&mdashbacteria tend to evolve resistance to antibiotics in such a way through mutations that would otherwise adversely affect membrane permeability.&rdquo 20

    Humans have been battling malaria for thousands of years. The advent of modern medicine provided us with a weapon to finally beat this ravaging parasite once and for all. Or so we thought. Unfortunately for us, malaria has been able to develop immunity to every drug we&rsquove thrown at it. For example, malaria quickly developed resistance to Atovaquone. All that was required to circumvent the effectiveness of this drug was a single point mutation at position 268 in a single malarial gene. The odds of developing this particular mutation are one in a trillion ( 10 12 ). While those odds would be difficult to overcome for most organisms (such as human beings or beetles), they are a cinch for malaria due to their staggering population sizes and reproduction rates. One trillion malarial parasites reside in each infected person, so odds are that at least one malarial parasite will develop resistance to Atovaquone in each and every infected person who takes the drug. Luckily for us, malaria is not always so lucky. Resistance to Atovaquone only develops in one out of three infected persons treated with the drug.

    We humans would not be outdone by malaria, so we concocted a new drug &ndash Chloroquine &ndash to help us defeat our microscopic enemy. To develop resistance to this drug, malaria would have to randomly experience two simultaneous and specific point mutations in a single protein. 21 While single point mutations are fairly common (1 per 100,000,000 nucleotides per the life of an organism), double-point mutations are extremely rare. 22 The odds of developing a double-point mutation like the one malaria would need to develop if it hoped to survive its battle with Chloroquine are 1 in 10 20 (one in a hundred billion billion). 23 If malaria populations were &ldquosmall&rdquo&mdashsay 1,000,000 parasites per infected person&mdashit would take one million years for malaria to meet those odds, but because there are so many malarial parasites (1 trillion per 1 billion people affected = 1,000,000,000,000,000,000,000 malaria parasites living in humans) they can, and have beat the odds. By chance alone one malarial parasite in every billionth infected person will gain resistance to Chloroquine. Once that resistant strand of malaria reproduces and spreads to other humans, it undermines the general effectiveness of Chloroquine.

    How long would it take mammals to develop a similar mutation by chance? Given our tiny population sizes and long reproductive cycles, it would take us twenty billion years! Not only is this 15 billion years more than the age of Earth, but it is 6 billion years more than the age of the universe itself! And what would we get for our long wait? A transformation from one species into another? No. A new biological system to help advance us toward the next stage of evolution? No. A new protein? No. We would simply get our existing cellular machinery broken in a manner that is fortuitously advantageous (micro-evolution of the devolution sort). This is the biological equivalent of using a TV to plug a hole in a dam. It may be a functionally acceptable solution to stave off immediate disaster, but it does nothing to build a new and improved dam.

    In his otherwise negative review of Michael Behe&rsquos book The Edge of Evolution, Sean Carrol agreed with Behe &ldquothat in most species two adaptive mutations occurring instantaneously at two specific sites in one gene are very unlikely and that functional changes in proteins often involve two or more sites.&rdquo 24 Microbiologist Allen Orr also agrees: &ldquoGiven realistically low mutation rates, double mutants will be so rare that adaptation is essentially constrained to surveying&mdashand substituting&mdashone-mutational step neighbors. Thus if a double-mutant sequence is favorable but all single amino acid mutants are deleterious, adaptation will generally not proceed.&rdquo 25 In other words, if a certain evolutionary change requires a double point mutation, we can be almost certain the organism will not evolve. The fact of the matter is that many features of advanced life would require double point mutations and greater, and thus we can be reasonably certain that macroevolution via random mutation is impossible.

    The HIV virus mutates at the evolutionary speed limit: 10,000 times faster than malaria. 26 Its genome is very small as well (nine genes versus thousands in malaria). 27 Its small size combined with a short reproduction time (1-2 days) and super-rapid mutation rate means every single nucleotide in the HIV genome will mutate 10,000 to 100,000 times in every infected person every day, and thus double point mutations like the one that made malaria immune to Chloroquine occur in every person every day. In fact, every possible double point mutation occurs in every HIV virus in every infected person every day. 28 Over the past several decades every possible combination of up to six point mutations has occurred in HIV somewhere in the world. If RM drives macroevolutionary changes in organisms, then we should observe macroevolution in the HIV virus since it experiences more mutations than any other organism. But we don&rsquot. HIV has run the gamut of all possible mutations to its genone, and yet with all of these mutations in a population of 100 billion billion viruses, no new cellular machinery has been created, and no new species has developed! HIV is still HIV. It still contains the same number of proteins, still performs the same function, and still binds to its host the same way it always has. There have been no significant biochemical changes. Even gene duplication has failed to produce any new biological information.

    Imagine for a moment that we were trying to determine whether it was possible to evolve a car into a submarine via naturalistic processes. The feat would require thousands of new mechanical systems and design changes, which in turn requires a lot of additional parts arranged in a very specific order. Let&rsquos say random parts are dropped from the sky once a day to help aid the process, but no intelligent agent is allowed near the car to select from among the parts or assemble them together in a particular order. If, after 100,000,000,000,000,000,000 parts were dropped from the sky over a period of 100 million years, the car remained virtually unchanged, what would you conclude about the theory that cars can evolve into submarines without the aid of intelligence if given enough chances to do so? Based on the empirical data you would probably conclude that it was highly unlikely, even if the time and parts were tripled in number. So what would you conclude if it was suggested that a car can evolve into a submarine using only 10% of those parts in 10% of the time? Surely you would conclude that such was impossible.

    This imaginary scenario is analogous to the debate over Darwinism. Darwinists ask us to believe that natural selection working on random mutations is capable of developing multiple new complex biological systems in a relatively short period of reproductive time in small populations, even though the empirical data has demonstrated that natural selection working on random mutations is incapable of developing even a single new protein in populations and periods of reproductive time that are magnitudes of orders larger.

    After observing trillions upon trillions of microorganisms over thousands upon thousands of generations we have discovered that RM has achieved very little in the way of biochemical advancement, and hence evolutionary significance. If RM cannot produce macro-evolutionary changes in bacteria, parasites, or viruses with their huge population sizes and short generation times, then surely there is no reason to think RM can do more in multi-cellular, sexual organisms such as mammals whose population sizes are orders of magnitude smaller, with generation times hundreds and thousands of times longer. As geneticist Francois Jacob said, evolution is a tinkerer, not an engineer. By tinkering around with a genome RM may get lucky and produce some functional advantage for an organism that helps it survive, but it does so at the expense of breaking existing biological information. While burning biological bridges may be functionally advantageous for stopping the advancement of the enemy, and hence one&rsquos survival, it is of no help in building new cellular machinery. Jerry Coyne and Hopi E. Hoekstra recognized this when they wrote, &ldquoSupporting the evo devo claim that cis-regulatory changes are responsible for morphological innovations requires showing that promoters are important in the evolution of new traits, not just the losses of old ones.&rdquo 29 Physicist Lee Spetner said it best, however: &ldquoWhoever thinks macroevolution can be made by such mutations is like the merchant who lost a little money on every sale but thought he could make it up on volume.&rdquo 30 The biochemical engineering needed to originate new kinds requires the aid of an Intelligent Engineer, not a blind tinkerer.

    Protein-Protein Biding Sites

    Most proteins work in teams of six or more. To fulfill their biological function each protein has to find its other partners among the thousands of proteins in the cell, and then assemble themselves together. This process of self-assembly is made possible due to binding sites located on each protein. To bind together, the three-dimensional surface shapes and the chemical properties of the proteins have to match (interlocking) at their binding sites. A wide rate of variability is needed to produce such specification, otherwise proteins would be able to bind together too easily, and thus they would be unlikely to bind with their intended partners. This would tend to produce large clumps of proteins in the cell, prohibiting most of them from carrying out their function, and making the organism less fit (or possibly even killing it).

    Unless every protein in a protein team evolved at the same time (which is beyond credulity), each protein&rsquos binding site would need to evolve independently of the others. The obvious question, then, is how these binding sites gained their specificity? What are the chances that the binding site of protein A would evolve the exact shape and chemical properties needed to complement the binding site of protein B, and the binding site of protein B would evolve the exact shape and chemical properties needed to complement the binding site of protein C, etc. for all the proteins in the protein team? The odds of evolving just one new binding site by chance alone are 1 in 10 20 . That is already inching toward the edge of what Darwinian evolution can produce, but since we need at least two independent binding sites for combination to occur, the odds are actually 1 in 10 40 . That is slightly more than the total number of cells that have ever existed on Earth in the past four billion years, and thus it is beyond the bounds of Darwinian evolution to produce. But it gets worse. Since proteins usually work in teams of six or more to fulfill a given biological function, the chances of forming the necessary binding sites required of the average protein team are 1 in 10 100 . That&rsquos 20 orders of magnitude more than all the elementary particles in the observable universe! And once again, for all this work, what is the reward? Only the binding together of proteins to perform a specific function within the cell. No new biological systems. No new organismal kinds. No macroevolution. 31

    Michael Behe sums up the problem this presents for Darwinism quite well:

    The development of protein features, such as protein-protein binding sites, that require the participation of multiple amino acid residues is a profound, fundamental problem that has stumped the evolutionary biology community until the present day&hellip. It is a fundamental problem because all proteins exert their effects by physically binding to something else, such as a small metabolite or DNA or other protein, and require multiple residues to do so. The problem is especially acute for protein-protein interactions, since most proteins in the cell are now known to act as teams of a half-dozen or more, rather than individually. Yet if one can&rsquot explain how specific protein-protein interactions developed, then it is delusional to claim that we can explain how anything that depends on them developed, such as the molecular machinery of the cell. It&rsquos like saying &ldquowe understand perfectly well how a car could evolve we just don&rsquot know how the pieces could get fit together.&rdquo 32

    The Fossil Record

    What about the fossil record? Doesn&rsquot it show evidence of evolution? No. While the fossil record suggests gradualism from simpler to more complex organisms, this in itself does not require Darwinian evolution. A design model could equally account for the data: God could have created different kinds of organisms over a long period of time, utilizing previous design patterns to create new, more complex organisms. Of course, this doesn&rsquot necessarily mean every distinct organism in the fossil record was independently created by God. Some could be the result of micro-evolution within kinds, producing distinct species.

    I think the Cambrian explosion reveals the superiority of the design model, however. For 85% of life&rsquos history life was simple, consisting mostly of one celled organisms and simple fauna, then in the equivalent of six geological minutes complex multi-cellular life burst on the scene, with 95% of all body plans that have ever existed emerging at that time, and without evidence of earlier, simpler ancestors. Darwin recognized the problem this posed to his theory. And 150 years later, that problem remains. Even Richard Dawkins has admitted, &ldquoThe Cambrian strata of rocks, vintage about 500 million years, are the oldest ones which we find most of the major invertebrate groups. And we find many of them already in an advanced state of evolution, the very first time they appear. It is as though they were just planted there, without any evolutionary history.&rdquo 33

    Secondly, there are large gaps in the fossil record and few plausible transitional forms. Organisms seem to just appear out of nowhere fully formed with no evolutionary history. If Darwinism is true, we would expect to find a fairly detailed account of each step in the macro-evolutionary process preserved in the fossil record (including thousands of ill-formed animals unfit for survival) just as Darwin predicted. What do we find? Nothing. New species appear suddenly with no trace of ancestors, persist for several million years, 34 then disappear in the same manner that they appeared: without a trace. Famed Harvard paleontologist Stephen J. Gould called this the &ldquotrade secret&rdquo of paleontologists.

    Third, the fossil record lacks any explanation of causal relationship between fossils. The evolutionary lines drawn in our textbooks constituting the evolutionary tree of life are supplied by the imagination of men who first presuppose the truth of common descent, not by the fossil record itself. 35 As Henry Gee, senior editor of biological sciences for Nature, wrote in 1999: &ldquoThe intervals of time that separate fossils are so huge that we cannot say anything definite about their possible connection through ancestry and descent. &hellip To take a line of fossils and claim that they represent a lineage is not a scientific hypothesis that can be tested, but an assertion that carries the same validity as a bedtime story&mdashamusing, perhaps even instructive, but not scientific.&rdquo 36 Thinking one can establish evolutionary relationships between such large gaps in the fossil record is like thinking one can reconstruct War and Peace based on the discovery of 13 pages, or thinking the discovery of Hawaii demonstrates that it is possible to walk from California to China! 37

    What one may think is an evolutionary relationship of descent between fossils may not be one at all. Consider how many species of dogs can be produced through artificial selection. Though all are dogs, they bear many morphological differences. Now imagine someone in the distant future who unearths fossil remains of these dogs without any knowledge of their origin. Given their morphological similarities, they might very well conclude that at least some of them evolved from others. It would be easy to see an evolutionary pattern between them based on their morphological similarities alone. While they may conclude that A evolved into B, B into C, and C into D, the fact of the matter is that there was no evolution at all. All of them are of a single dog kind all of them were created within a few hundred or thousand years of one another and none of them originated through the Darwinian process of random mutation and natural selection (they were created by artificial selection through breeding). Couldn&rsquot evolutionary paleontologists be making similar mistakes in their assessment of the fossil record? Couldn&rsquot it be that what we perceive as an evolutionary relationship between fossils is nothing more than various species of the same general kind? It is highly subjective, if not illegitimate, to claim evolutionary relationships between fossils based on morphology alone.

    That morphology is not an adequate basis for determining ancestry has also been demonstrated by molecular studies. These studies yield evolutionary trees quite different from those constructed from morphological analysis alone. As Masami Hasegawa et al wrote in the Journal of Molecular Evolution, &ldquoThat molecular evidence typically squares with morphological patterns is a view held by many biologists, but interestingly, by relatively few systematists. Most of the latter know that the two lines of evidence may often be incongruent.&rdquo 38 A good example of this is the story of horse (equid) evolution. A recent study in the eminent journal, Proceedings of the National Academy of Sciences,not only discovered that a DNA-based evolutionary tree is inconsistent with a morphologically-based evolutionary tree, but also that some equid fossils thought to be different species based on their morphological differences turned out to be variations of the same species when their DNA was examined. 39 This is a real-life example demonstrating the reality of the error I spoke of in the previous paragraph.

    Fourth, while the fossil record cannot be ignored when exploring the question of biological history, it is not sufficient in itself for demonstrating macro-evolution. It&rsquos not enough to say that because fossil B looks similar to fossil A that precedes it and fossil C that follows it, it must be a transitional form between the two. While that is a possibility, one needs to do more than just point to morphological similarities (homology) between fossilized organisms to demonstrate macro-evolution. One needs to lay out a plausible biochemical pathway that would produce the hundreds of thousands of morphological/systemic/functional transformations needed to evolve one kind of organism into another, and show that this pathway could be traversed in the amount of time required by the fossil evidence. 40 Nobody is doing this. One has to just take it on faith in Darwinism that such transformations are possible. Given what we&rsquove discovered about the limits of RM+NS to generate the required biological information, that faith would have to be blind. RM+NS cannot produce the types of changes needed to produce the diversification of life we observe in the fossil record.

    For the Darwinian explanation of the fossil record to be compelling, it needs to do more than account for the general trend toward higher complexity. It needs to account for the sudden emergence of complex multicellular life, the sudden emergence of nearly all phyla, the lack of intermediates, and long periods of stasis. If Darwinism cannot provide an adequate empirical explanation for this phenomenon, then it should not be considered the best explanation of the fossil record. Indeed, the fossil record better fits the notion of progressive creation events by a designing intelligence. Not only can Intelligent Design equally explain the gradual and increasing complexity found in the fossil record, but it can also explain why it doesn&rsquot begin simple, how so many new phyla appeared in such a short period of geological time, why it lacks transitional forms, and why stasis&mdashnot change&mdashis the norm.

    The scientific evidence is not confirming the neo-Darwinian synthesis, but falsifying it. The empirical evidence points to the regular involvement of an Intelligent Designer in the history of life. If modern science had not committed itself to the philosophy of methodological naturalism (in which only naturalistic explanations are allowed for natural phenomenon) Darwinism would be laughed out of court for paucity of evidence.
    Darwinism has prevailed, not because it is the best explanation of the data, but because it is the best naturalistic explanation of the data &ndash the only kind of explanation many scientists are willing to consider based on their a priori commitment to naturalism. If one begins by assuming philosophical or methodological naturalism, then something like Darwinism has to be true even in the absence of evidential confirmation and explanatory value. As Richard Dawkins has admitted, &ldquoEven if there were no actual evidence in favor of the Darwinian theory&hellipwe should still be justified in preferring it over all rival theories.&rdquo 41 (emphasis mine) Why? Because Darwinism is a naturalistic theory, while others are not. Darwinism wins the day, not because it has prevailed over the competition, but because it has eliminated the competition by definitional fiat, rooted in a philosophical bias. When you define your league so narrowly that only one team is allowed to play, is it any surprise that you win the World Series?


    Hand-washing resistant bacteria. Will they evolve one day? - Biology


    1. Science Highlight — Fighting Antibiotic Resistance: New Drug Target Mapped
    (contact: Robert Scott, [email protected])

    Antibiotics and the bacteria they attack are engaged in a constant race to out-evolve one another. An antibiotic is effective against specific bacteria only so long before the random mutations that all bacteria undergo make them resistant to that particular drug. Recently, scientists from the University of Georgia, Utah State University, and Guilford Pharmaceuticals carried out studies at SSRL that could enable drug designers to pull ahead, at least for a while, by developing a new class of antibiotics.

    Their work explored a novel antibacterial target: a step in the recipe most bacteria use to create the rigid wall that surrounds and protects individual bacterial cells. Two important components of the cell wall, mDAP and lysine, are synthesized in bacteria by the enzyme DapE. Deleting the gene that encodes DapE has been shown to be lethal to certain bacteria, including the strain that causes stomach ulcers and that appears to be a major cause of stomach cancer, so inhibiting the DapE enzyme looks like a promising approach for drug designers. Because mammals use a different recipe to make their cell walls, an antibiotic that inhibits the DapE enzyme should be toxic to bacteria but not to human cells.

    The researchers used a technique possible only with synchrotron light (analysis of extended x-ray absorption fine structure or EXAFS) to map the atomic neighborhood of the chemically active part of the DapE enzyme. This information is important for identifying a chemical component that can lock onto this site and prevent the enzyme from doing its job in production of the cell wall. The investigators also obtained additional information useful in drug design: a view of enzyme bound to inhibiting molecules and a glimpse of the enzyme in action.


    2. The Structure of the First Coordination Shell in Water
    (contact: Anders Nilsson, [email protected])

    Water is the key molecule for our existence on this planet and it is involved in a great number of biological, geological and chemical processes. Knowledge about the hydrogen-bonded network structure in water is essential for understanding its unusual chemical and physical properties. In its condensed phase, ice (Ih) e.g., each water molecule is coordinated by four others in a semi-tetrahedral arrangement forming an ordered crystal structure. In contrast, in liquid water a statistical distribution of different coordinations can be assumed due to the dynamical motion of the atoms causing the hydrogen bonds to break and reform on a picosecond (ps)-time scale. In a recent report, Wernet et al. [Science Express Reports, 10.1126/science.1096205 (2004)] studied the first hydration shell of a water molecule in bulk liquid water by probing its electronic structure using X-ray Absorption Spectroscopy (XAS) and X-ray Raman Scattering (XRS). From carefully designed experimental models as well as theoretical spectra simulations, with results contrary to molecular dynamics simulations, Wernet and coworkers conclude that the local surrounding of a water molecule in liquid water resembles that in the topmost layer of ice, i.e., it is characterized by a substantial number of broken hydrogen bonds. The results of the study shows that water, on the probed sub-femtosecond time-scale, consists mainly of structures with two strong hydrogen bonds, one donating and one accepting, compared to the four-hydrogen-bonded tetrahedral structure in ice. This implies that most molecules are arranged in strongly hydrogen-bonded chains or rings embedded in a disordered cluster network connected mainly by weak hydrogen bonds. See http://www-ssrl.slac.stanford.edu/structureofwater.html for links to the paper in Science, press release, and a more detailed description of the results.


    3. User Operations Update
    (contact: Cathy Knotts, [email protected])

    Several more beam lines have opened during the past month including 11-1, 11-2, 11-3, 7-2 and 2-3. SPEAR3 has delivered an average of 95% of the beam time scheduled for users so far, this despite a one-day down caused by an RF power failure in the injector earlier this week. Top offs are still being scheduled four times a day at 6 am, 12 pm, 6 pm and 12 am, but the fill time is only about 3 minutes. One user has commented "The fills are too short to even get a cup of coffee, much less go out for a meal". Announcements will be made before each fill, and users may request a slight delay on the fill time to coordinate their scans and maximize their data taking. SPEAR status updates are available on the website:
    http://www-ssrl.slac.stanford.edu/talk_display.html

    Due to issues related to the SLAC electrical power contract, the user run will end on July 31 at 10 pm, rather than August 2 at 6 am as originally projected. The SPEAR operating schedule is available on the website:
    http://www-ssrl.slac.stanford.edu/schedules/


    4. SPEAR3 Improved Performance Benefiting Users
    (contact: Piero Pianetta, [email protected])

      John Bargar and Joe Rogers (SSRL) have collected data on BL11-2 that confirm that electron beam stability is vastly improved in comparison to SPEAR2. In fact, SPEAR3 motion is about 15 times smaller than with SPEAR2. Electron source stability will fundamentally improve data quality at all beam lines, and is absolutely crucial for micro-beam station performance.


    Watch the video: Hvordan hindre antibiotikaresistens? (September 2022).


Comments:

  1. Conaire

    Author, read comments, all spam

  2. Barclay

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  3. Saunders

    In my opinion, you admit the mistake. I can prove it.



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