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Unity and Diversity of Life
All cellular organisms share certain traits as a result of sharing (or “descending from”) a common ancestor (the first primitive prokaryotic cells). Yet the incredible diversity of living organisms is astounding. How did such diversity arise?
The diversity of life is explained by evolution, a change in the genetic makeup of a population of organisms.
The “raw material” of evolution is genetic variability, the genetic differences between individuals of a population of organisms. How does genetic variability arise?
Genetic variability arises through random mutations, changes in the nucleic acid sequence of organisms, horizontal gene transfer in microbes and sexual recombination.
Random mutations: These mutations usually occur when the enzymes which copy genetic information before a cell divides make a mistake. As an example, the enzyme DNA polymerase should copy the DNA sequence below precisely.
DNA base abbreviations:
A=adenine T=Thymine G=Guanine C=cytosine
Original genetic info, DNA base sequence of double stranded DNA
A-T- C- G- G
T- A- G- C- C
DNA polymerase should make a precise copy of the DNA before the cell divides such that each “daughter” cell receives a precise copy of genetic information from the parent cell:
A-T- C- G- G
T- A- G- C- C copy 1
A-T- C- G- G /T- A- G- C- C --- DNA polymerase copies
Original DNA A-T- C- G- G
T- A- G- C- C
When the original cell divides, both “daughter” cells will receive one copy of the DNA, exact copies of the DNA from the “parent” cell
One source of genetic variability occurs when DNA polymerase makes a mistake copying the original DNA as shown below:
A-T- C- G- G
T- A- G- C- G* ,<-mistake=mutation copy 1
A-T- C- G- G /
T- A- G- C- C --- DNA polymerase copies
Original DNA A-T- C- G- G
T- A- G- C- C
In this case, DNA polymerase made a mistake in copy #1 (instead of a “C”, it used a “G”). This is a mutation, a change in the DNA sequence. As a result, the mutated gene might encode information for a different variety of protein. This different protein could change some feature of the “daughter cell” which receives the mutant DNA copy. This mutant organism might be a better competitor compared to “normal, non-mutant” member of its population (or the mutant might be less able to compete with its “normal” colleagues).
If resources are limited, “variants” or mutants which are better competitors will survive in higher numbers than their non-mutant neighbors. The mutants will have more offspring than the non-mutant members of the population which are weaker competitors. The mutation which permitted the variant to compete better will be passed on to its offspring. Over time, the mutant form of the genetic information will be carried by a greater proportion of the surviving population, another way of saying the frequency of the mutant gene increases in the population. Thus the gene pool or genetic makeup the population has changed over time and the population of organisms has “evolved” (and the population becomes better adapted to the environment over time) .
This mechanism above describing “how” evolution occurs is called “natural selection”, a concept developed by Charles Darwin and Alfred Wallace in the 1800’s. (Darwin and Wallace were not the first people to describe evolution, but they were the first describe the process of natural selection).
Darwin and Wallace’s explanation of evolution by natural selection is based on 5 assumption (source: Keeton and Gould’s Biology 4th edition, Norton Publishers)
1. Many more individuals are born in each generation than will survive and reproduce (limiting environmental resources, competition for resources)
2. There is variation among individuals of a population.
3. Individuals with certain characteristics have a better chance of surviving and reproducing than individuals with other characteristics.
4. Some of the differences resulting in differential survival and reproduction are heritable
5. Vast spans of time have been available for change
Natural selection vs Artificial selection
When “nature” chooses which variants are best at competing for natural resources, and thus will survive and reproduce at higher rates than other variants , “natural selection” occurs. However if humans selectively breed organisms for specific traits, or if humans purposely change the environment (for example through overuse of antibiotics), “artificial selection” occurs. The overuse/misuse of antibiotics worldwide has artificially selected for a growing number of antibiotic resistant bacteria.
Evolution of antibiotic resistant bacteria
As bacteria reproduce so quickly, it does not take “vast spans of time” for their populations to evolve. Antibiotic resistance can evolve within a few years (even within a few weeks) within some populations of bacteria.
Evolution of variant strains of RNA viruses: HIV and influenza
Cellular organisms all have DNA as their genetic information. The enzyme which copies DNA, the DNA polymerases, have “high fidelity”, that is these enzymes make relatively few mistakes because they have the ability to “edit or proofread” their work and correct many of their mistakes. Mistake rates fro DNA polymerase are approximately one incorrect nucleotide per 108-109 nucleotides.
In contrast, some types of viruses (acellular pathogens) use RNA as their genetic information. The enzymes which copy RNA, the RNA polymerases, lack the ability to correct mistakes, therefore RNA polymerases have a very high mistake rate (one incorrect nucleotide every104-105 nucleotides) . Consequently many RNA viruses such as influenza virus and HIV, have very high mutation rates thus “populations” of HIV and influenza viruses evolve quickly. The high mutation rate of these viruses results in rapid drug resistance and huge challenges in vaccine production.
Natural Selection in a “nutshell”
1. Each species produces more offspring than can survive
2. The offspring compete with one another for limited resources
3. Organisms in every population vary
4. Organisms with most favorable traits/variations are most likely to survive and produce more offspring
Result:…..consequently variant genes “spread” through the population over time, genetic makeup of population changes and population changes/evolves over time=”Evolution”
Horizontal Gene Transfer in Bacteria
Transfer of genetic material between prokaryotes: transformation, transduction, conjugation
I. Genetic Recombination and Homologous Recombination an exchange of DNA sequences by crossing over- permits integration of “foreign” homologous DNA into bacterial host chromosome. Replaces bacterial alleles w/ “foreign” alleles.
1. “Foreign” single stranded homologous chromosomal DNA aligns with homologous sequences of host bacterial chromosomal DNA
2. DNA fragment of host DNA excised, replaced by foreign DNA sequence-alters cells genotype (“native” allele is replaced w/ a foreign allele)
3. Requires many enzymes including recombination enzymes/proteins, nucleases, ligases
II. Transformation: uptake of “naked” DNA from environment by competent bacterial cells.
1. plasmid DNA or chromosomal DNA
2. Some bacterial strains naturally competent. Special surface proteins recognize and take-up closely related naked DNA from environment (recall Griffith’s experiments w/ Streptococcus pneumoniae). Other bacterial strains can be made competent by treatment with chemicals (ex cold + calcium chloride treatment used in lab to create competent E. coli cells; permitted uptake of double stranded plasmid DNA)
3. Competent Streptococcus pneumoniae permit passage of single stranded DNA through cell membrane (2nd strand is usually degraded).
4. When competent cell is transformed with DNA, the cells are referred to as “transformants. Chromosomal DNA may undergo genetic recombination with bacterial DNA if homologous sequences are present.
III. Transduction. DNA transfer process in which bacteriophages carry DNA from one bacterium to another bacterium. 2 types: generalized and specialized.
1. Generalized transduction:(bacterial genes transferred at random) Recall lytic reproductive cycle. Towards end of cycle, bacterial chromosomal DNA is accidentally packaged into phage heads/capsids instead of phage DNA. This creates a defective phage as it lacks its own genetic material, yet it can still be released, attach to new bacterium and inject the DNA into a new host bacterium. This DNA may replace the homologous region of the bacterial chromosome.. The bacterial cell now carries recombinant DNA.
2. Specialized transduction (only specific bacterial genes are transferred). Requires temperate bacteriophage. Phage DNA integrates into host bacterial chromosome usually at specific site. Later prophage may be induced to enter lytic cycle. When prophage excises from chromosome, sometimes take small stretch of adjacent bacterial DNA. Bacterial genes are packaged w/ phage DNA and injected into new bacterial host.
IV. Conjugation. Direct transfer of genetic material between 2 bacteria which are temporarily joined. Model uses E. coli (gram positive bacteria use slightly different process).
1. One-way transfer of DNA: donor cell (male) transfers genetic material to recepient cell (female)
2. Male uses protein appendages, hollow sex pili, to attach to female
3. Temporary cytoplasmic bridge forms between 2 cells, providing path for transfer of DNA
4. “Maleness’, ability to form sex pili and transfer DNA during conjugation, results from presence of special DNA sequence called F factor=Fertility Factor . F factor may exist integrated into chromosome or as a plasmid, therefore it is an episome (episome= genetic element which can replicate either as a plasmid or as part of bacterial chromosome; temperate viruses such as lambda also qualify as episomes).
5. Recall plasmids are extrachromosomal, self-replicating DNA elements which usually carry “extra’ genes. These genes can confer survival advantages for bacteria living under stressful conditions. For example, “R plasmids” are plasmids carrying genes for antibiotic resistance and permit host cells to survive in presence of antibiotic pressure. F factor facilitates genetic recombination which could be advantageous in a changing environment which no longer favors existing strains of bacteria (Campbell, Biology 5th ed)
6. F plasmid: The F factor in its plasmid form is called the F plasmid. Consists of approx. 25 genes, most involved in sex pilus production.
a. F+ cells (males) contain F plasmid; F plasmid is usually replicated and passed to daughter cells. F+ condition is “contagious” as it can be passed to female cells, converting them to F+ males following conjugation
b. F- cells (females) lack F plasmid
c. F plasmid is replicated in male and a copy is passed to female, converting her to F+ male. Only F plasmid copy is transferred during F+ x F- conjugation
7. Hfr and bacterial gene transfer during conjugation
a. if F factor is integrated into bacterial chromosome, bacterium is referred to as Hfr cell (High frequency of recombination)
b. Hfr acts as a male, forms sex pilus, copies F factor, starts to transfer copy of F to F- partner, yet now F factor also takes a copy of some of bacterial chromosomal DNA with it
-temporarily, female is diploid until genetic recombination occurs and segments of DNA are exchanged (excised DNA is degraded)
-Female becomes recombinant cell; usually mating is interrupted before entire chromosome and F factor are transferred therefore she usually remains female
V. Resistance Plasmids and Transposons
1. R =resistance plasmids, carry genes for antibiotic resistance and/or resistance to heavy metals e.g. mercury resistance. Example enzymes to destroy antibiotics. beta-lactamases destroy beta-lactam ring of penicillin, ampiciilin and related antibiotics, mercury reducatase genes.
2. R plasmids may carry multiple antibiotic resistance genes and can be copied and transferred between bacteria via conjugation and transformation
3. Some R plasmids carry 10 antibiotic resistance genes; evolution thought linked to transposons
4. Transposons are transposable genetic elements, pieces of DNA which can move from one location to another (Barbara McClintock’s “jumping genes”1940’s-50’s; Nobel prize 1983 age 81). Some say transposons (“Tn’s”) never exist independently some gram-positive Tn’s may violate this rule.
5. Transposons may have moved multiple antibiotic resistance genes to R plasmids
6. Insertion sequences (IS)-simplest transposons. Carry 1 gene only for enzyme transposase bracketed by inverted repeats, upside down, backwards versions of each other . Transposase binds to inverted repeats and recognizes target sites. Transposase cuts target sequences and inserts IS. “Cut and Paste Transposition”
7. Composite transposons: Additional genes e.g., for antibiotic resistance sandwich between 2 IS. Probably involved in evolution of R plasmids
3 Mutations Evolution and Natural Selection - Biology
The process of biological evolution can be accurately defined as “descent with modification.” This definition includes microevolution (changes in allele frequency of a population over time) and macroevolution (the descent of different species from a shared common ancestor over many generations). Evolution relies on four processes that function as the basic mechanisms of evolutionary change:
- Mutation. Mutations are the ultimate source of variation in a population, resulting in changes in the genetic makeup of an individual.
- Migration. The allele frequency of a population can change if members of an existing population leave, or new members join.
- Genetic Drift. Genetic drift happens when allele frequencies change due to purely random factors. For example, if a person accidentally stepped on a population of beetles and randomly killed all the brown beetles in the population, the allele frequency of the population would certainly change, but the cause of the change is completely random. This is an example of genetic drift. It is most significant in small populations.
- Natural Selection. Charles Darwin based his theory of natural selection as the driving force for evolution from the following observations:
- Reproduction. Species reproduce in excess of the numbers that can survive.
- Variation. All sexually reproducing species vary in characteristics.
- Heredity. Traits can be passed from one generation to the next.
- Fitness. Those individuals with hereditary characteristics that have survival value, i.e., improved fitness, are more likely to survive and reproduce compared with less fit individuals. Be careful here, because the word “fitness” does not refer to physical fitness or healthiness! This word is being used in a very specific way to mean “successful reproduction.” Fit individuals make more babies. This is not necessarily true of our common use of the word!
If these four processes are coupled with reproductive isolation, then speciation (the formation of a new species) can occur. Reproductive isolation occurs by some mechanism that can isolate diverging populations so as to prevent interbreeding. Given sufficient time, a population that is isolated from the original population can diverge physically and/or behaviorally to the point where it is a distinct species. There is a variety of isolating mechanisms that can prevent gene flow from occurring. One example is the presence of geographical barriers such as mountain ranges or islands that prevent gene flow between separated populations.
Evolution is the Source of New Species
All species of living organisms evolved at some point from a common ancestor. Although it may seem that living things today stay much the same from generation to generation, that is not the case: evolution is ongoing. Evolution is the process through which the characteristics of species change and through which new species arise.
The theory of evolution is a unifying theory of biology, meaning it is a framework within which biologists ask questions about the living world. Its power is that it provides direction for predictions about living things that are borne out in experiment after experiment. The Ukrainian-born American geneticist Theodosius Dobzhansky famously wrote that “nothing makes sense in biology except in the light of evolution.”  He meant that the principle that all life has evolved and diversified from a common ancestor is the foundation from which we understand all other questions in biology. This chapter will explain some of the mechanisms for evolutionary change and the kinds of questions that biologists can and have answered using evolutionary theory.
Natural Selection is a Mechanism of Evolution
The theory of evolution by natural selection describes a mechanism for species change over time. That species change had been suggested and debated well before Darwin. The view that species were static and unchanging was grounded in the writings of Plato, yet there were also ancient Greeks that expressed evolutionary ideas.
Natural Selection and the Human Lineage
In the last two posts in this series, we examined how natural and artificial selection shaped the dog genome over time. One example that we discussed was the duplication of the gene for the amylase enzyme in dogs. Recall that amylase is a protein enzyme produced in the pancreas that breaks down starch. This duplication increases the amount of amylase enzyme secreted into the dog’s digestive system, and in turn allows dogs with the duplication to derive more nutrition from the high-starch diet they were scavenging (or receiving) from humans. Since it provided a nutritional benefit to the dogs that carried it, these dogs would reproduce at a slightly higher average rate than dogs without it.
The original duplication event would have occurred in one dog as an error during chromosome replication. Over many generations, the “duplicated amylase gene” variant would become more and more common in the population, since dogs with it would leave more offspring, on average, than dogs without it. Later, additional duplications of the original duplication would arise, giving some dogs an even greater amount of amylase. Eventually, the original non-duplicated variant would disappear from the dog population altogether, though it would persist unchanged in wolves. Now, note well—there is a reasonable probability that a similar duplication has occurred in a wolf at some time—but it was not selected for, since wolves would derive no benefit from an increased ability to break down starch. Such a duplication, if it occurred, would have been lost from the wolf population it arose in.
To summarize, the overall process has a number of steps that can be generalized:
Random mutation: “random” can be a theologically loaded word, but for our purposes, we will use the biological definition of “random”: that the mutation event (the duplication) was “random with respect to fitness.” What this means is that the mutation event was not connected to, nor foreseeing, the benefit that it would provide. It was simply one of many mutations that occurred in ancestral dogs. We know about it because it has been passed down to dogs in the present day (given its selective advantage). Many other mutations that had no effect (or a negative effect) also occurred, but these have not been selected for. I’ve often encountered the misconception among non-biologists that mutations are always harmful, or always remove functions and information. As this example illustrates, however, in many cases mutations can be beneficial, add gene copies, and new functions and information to the organism as well. In a later post in this series, we’ll explore a wide range of different mutations, and examine how they can add or remove functions—but for our present purposes, it’s enough to underscore that not all mutations are harmful, and some are decidedly beneficial.
Natural selection: once the new, duplicated variant arose, it provided a reproductive advantage compared to the non-duplicated version. Any time one variant reproduces at a greater rate than another, natural selection is happening. The duplicated variant became more common in the population (since dogs with it reproduced, on average, more often than dogs without it). Oftentimes natural selection is viewed as a sudden, dramatic slaughter of the “unfit” with only the new, “greatly improved” individuals surviving. This is a popular, but inaccurate understanding—natural selection can be as simple as a slightly increased reproduction rate over many generations. In this case, dogs without the duplicated amylase genes continued to reproduce, but just slightly less frequently than dogs with the duplication.
Change in average characteristics within the population over time: at the start of the process, only one dog had an increased ability to produce amylase. By the end of the process, many, many generations later, all dogs had this ability, because they had all inherited the duplicated version (i.e. it had replaced the non-duplicated variant in the population). Over time, the average ability of the population to digest starch improved. Again, one common misconception of evolution is that it is a dramatic, sudden process, with offspring that differ greatly from their parents. Not so—evolution is a gradual process, with average characteristics shifting slowly over time within a breeding population.
In summary, mutations introduce variation, and not all variants reproduce at the same frequency in a given environment (i.e. the environment acts as a selective filter). Over many generations, these effects can shift the average characteristics of a population.
Source: Scott Bauer, USDA ARS
Has natural selection shaped the human genome?
Sometimes students, having learned about natural selection in other organisms, balk at the notion that this process was involved in our own origins. Despite this hesitation, there is very strong evidence that our own lineage has been subject to natural selection over its long history leading to our species. One example of this evidence comes from the history of our own amylase genes. The story shares similarities to what we have seen for the dog lineage, but also has some interesting differences.
Unlike dogs, humans have two distinct types of amylase genes. Both types have the same enzymatic function (breaking down starch), but they are produced in different locations in the body. One of the types is produced in the pancreas, just like the equivalent enzyme in dogs. Unlike dogs, however, humans have amylase in our saliva as well. This “salivary” amylase works quickly enough that we perceive starchy foods as sweet when we chew them—the amylase enzyme goes to work on the starch, breaking it down into glucose quickly enough for us to taste it. Studies have also shown that salivary amylase continues breaking down starch right through our stomachs and on into our intestines—thereby increasing the amount of glucose we can extract from foods rich in starch.
As you might expect, the human pancreatic and salivary amylase genes sit side-by-side in our genomes, and show the clear signs of being duplicates of each other.* All mammals have pancreatic amylase genes, but only some, such as humans, have salivary amylase genes. This means that the ancestral state was a single pancreatic amylase gene, and the first duplication event produced a second copy, just like what we have seen for dogs. This doubling of pancreatic amylase would likely have been an advantage and come under natural selection in a similar way to what we have seen for dogs. The fact that humans and other great apes share the same duplication event indicates that this event took place in the common ancestor of these species, and thus on the order of 16-20 million years ago.
Once the two pancreatic amylase genes were present in our ancestral lineage, a second event occurred that altered one of the copies: an endogenous retrovirus inserted into the genome next to one of the copies. (Retroviruses are viruses that insert their own genome into the genome of their hosts as part of their infection cycle. Endogenous retroviruses insert into the genome of reproductive cells, such as eggs or sperm—and once inserted, they can persist at a specific spot in a host genome and be passed down from generation to generation.) This retrovirus insertion event altered the DNA sequence that controlled when and where the amylase protein was made—and instead of being made in the pancreas, the altered copy began to be made in salivary glands instead.** Over time, this new combination (one pancreatic copy and one salivary copy) came under natural selection and replaced the previous version that gave rise to it (two pancreatic copies).
So, the story of the human amylase gene cluster thus far shows clear signs of repeated mutations (such as duplications) coupled with natural selection to produce the genes that we see in humans today. Of course, if humans were directly created without common ancestry, there would be no need to create these genes directly and then embed within them the evidence of a convoluted history—yet what we see, time and time again, is the clear evidence of mutation and natural selection. It seems that God was pleased to create this aspect of our biology slowly, through what we perceive as a “natural” process—but of course, what we perceive as “natural” is merely the consistent outworking of God’s ordained and sustained providence that is amenable to scientific investigation. As we became human, and shifted our diet towards agriculture and starchy foods, this God-given mechanism allowed us to take advantage of the shift in our environment.
Previously, we described some of the early steps on the path to the present-day human amylase gene cluster, and the role that natural selection played in the process. Having set the stage, we’re now ready to continue the story—and, as we’ll see, it was a long and winding path from this starting point to arrive at what we see in the present day.
As you will recall, the early evolutionary steps in this process (a) duplicated the original human pancreatic amylase gene, and (b) later changed the activity of one of the copies, such that it was no longer made in the pancreas, but rather in saliva. We further noted that this new variant (which we can abbreviate as “1 pancreas / 1 salivary”) came under selection and replaced the “2 pancreas / 0 salivary” variant that it arose from. Having arrived at this point our ancestors would have had amylase enzyme secreted into the small intestine by the pancreas, but also a new function, amylase secretion from the parotid gland into saliva. This salivary amylase would have provided an advantage in an environment with access to starchy foods, since amylase can break down more starch into glucose with enzymes made in both locations than it can with merely two copies made in the pancreas.
This was not the end of the story, however: the stage was now set for further mutational steps that would also be selected for.
What happens next is more straightforward duplication events, similar to the duplication events we have seen before. This time, however, the duplication copies the newer salivary amylase gene. This duplication results in yet another new variant (1 pancreas / 2 salivary) that is selected for as well, since it is an improvement over the (1 pancreas / 1 salivary) variant it arose from. Later on, there is another duplication that spans both salivary copies to give a combination of 1 pancreas / 4 salivary copies. At this point there are five distinct gene copies, all side by side in the genome, and this variant also replaces the previous version due to selection.
The next stage, however, has a twist. Recall that it was the insertion of a retroviral DNA sequence that originally converted the second amylase gene copy from a pancreas enzyme to a salivary enzyme. This retrovirus sequence was copied along with the rest of this gene when it was duplicated, and at this point is still present in each of the four salivary gene copies. Later, the retrovirus excises itself from one of the four salivary copies (leaving only a small “footprint” behind), reverting it back to production in the pancreas. This results in a new (2 pancreas / 3 salivary) variant. This new variant also comes under selection and replaces the (1 pancreas +4 salivary) variant that it arose from, since the doubling of the pancreas enzyme offers an advantage at this point, even if it comes at the expense of one of the salivary genes. The salivary copy that was converted back to a pancreatic gene retains a “scar” of once having been a salivary gene—with a genetic “there-and-back again” tale to tell.
If this all seems a little convoluted, I don’t blame you—it is convoluted. But that is the point—this is the convoluted history that is written into this region of our genomes. It ably demonstrates that we have been shaped by mutation and natural selection. These are the very same types of mutation and selection events that scientists have observed in real time in experimental organisms, and they demonstrate that random mutation (again, random in the biological sense, as we discussed yesterday) is quite capable of producing new genes with new properties, and that natural selection is able to shift a population over to new, advantageous variants that arise.
And on it goes, even to this day
At this point you might think that the story was over, and that all humans now have the “2 pancreas / 3 salivary” version of the amylase gene cluster. What is interesting is that this is not actually the case. Some humans have even more copies of the salivary amylase genes – individuals with up to a staggering 10 salivary copies side-by-side have been identified. At the other end of the scale, some humans have less than the “standard” 3 copies, perhaps just two or even only one. These variants arose as deletions from the “standard” 2 pancreas / 3 salivary arrangement. In other words, humans are hugely variable for the number of salivary amylase genes – as a population, we are not uniform. Some of us have more amylase in our saliva than others.
Variation, of course, is only one part of the recipe for evolutionary change. In order to shift average characteristics of a population over time, natural selection needs to be acting on that variation. To test the hypothesis that natural selection is acting on human salivary amylase copy number variation, researchers have looked to see if human populations using a high starch diet have different copy numbers, on average, than human populations using a diet low in starch.
The results are striking, and support the hypothesis that natural selection is acting on copy number variation in modern humans. In populations that have historically used a high starch diet, the average salivary amylase copy number is significantly higher than for populations that historically use a low starch diet. Detailed molecular analysis of the genomic region containing the amylase gene cluster in populations using a high-starch diet also showed signs of selection, in that they had greatly reduced variability (as one would expect if selection was acting). This reduced variability was not seen in these same populations for other genome regions with variable copy numbers. Taken together, these results support the hypothesis that natural selection is at work on the amylase gene cluster region in human populations. So, it seems that this story is still unfolding—and that we can observe a snapshot of the process at our moment in history.
Completing the circle: from man to dog
Two further lessons we can draw from this example require us to think back to the similar process that occurred during dog domestication. In dogs, there are numerous copies of pancreatic amylase genes, and dogs are currently variable for the number of copies they have. These duplication events in the dog lineage owe their selective advantage to the prior amylase duplication events in the human lineage. The human duplications were part of improving our reproductive success as we shifted over to a diet with greater starch content. While humans made the shift, dog populations associated with humans experienced a similar shift in environment—they, too, had access to greater amounts of starch.
This altered environment provided a selective advantage to variants within the dog population that, like their human companions, could benefit from increased starch consumption. The shift in the first species (humans) has a direct link to the shift in a second species (dog). This is an example of what is known as co-evolution: where two species in close contact act as major features of the other species’ environment, and selective changes in the one species shift what is advantageous for the other species. This human / dog amylase story is also an example of evolution “repeating” itself in two independent lineages—in this case, similar gene duplication events that boosted the amount of pancreatic amylase independently in dogs and humans. The technical term for this is convergent evolution—evolutionary paths that arrive independently at the same “solution” in two lineages.
While we will look at co-evolution and convergent evolution in more detail in later posts, it is worth noting these features now, while this example is fresh in our minds. The take-home message here is simple: evolution is not just a chance-based process, but also one that is, at least to a certain degree, repeatable. In part, this repeatability is based on organisms encountering similar environments, and these environments selecting for similar outcomes in both species. In the case of species in close contact, a shift in one species can open up a new opportunity for the second species.
In the next post in this series, we’ll examine further details of how genetic variation arises in populations, and how selection may or may not act on it.
Notes & References
* Space does not permit a detailed discussion of the features of the various amylase gene copies that reveal their duplication and / or mutation history. Readers interested in the details can find them in the following published papers:
Samuelson, L.C. et al., (1996). Amylase gene structures in primates: retroposon insertions and promoter evolution. Molecular Biology and Evolution 13 767-779. (link)
Meisler, M.H. and Ting, C.N. (1993). The remarkable evolutionary history of the human amylase genes. Crit Rev Oral Biol Med 4 503-509. (link)
** For readers who follow the Intelligent Design literature closely, the production of the salivary-specific promoter sequence is what ID proponent Michael Behe would describe as a “gain-of-Functional Coded elemenT” (FCT) mutation. The promoter sequence is derived partially from the retrovirus sequence and partially from the DNA sequence next to the insertion site. As such, neither the virus nor the host DNA contain a FCT that can produce expression in the salivary gland. Their combined sequences create the FCT de novo, and this FCT is lost when the virus excises from the one copy, reverting it to expression in the pancreas. Readers may recall that I have critiqued Behe’s arguments based on FCTs in a previous five-part series.
4. The Reach of Epigenetic Research in the Life Sciences
4.1. Intragenerational and Transgenerational Epigenetics
The first phase of the survey determined the relative frequency of the occurrence of intragenerational vs. transgenerational epigenetic papers. The actual use of these two specific terms as the secondary search term was not productive: only slightly above 1% of all epigenetic papers actually contained either or both of these adjectives. Subsequently, five major categories of epigenetic papers were formed for this survey. Epigenetic papers including the terms “mechanism”, 𠇍isease” and velopment and ageing” (and their related topics) were considered to be more representative of an intragenerational perspective, while epigenetic studies, including the terms 𠇎volution” and “inheritance”, were considered to be more representative of epigenetic papers with a transgenerational component to them (however little that might be) Of course, there are transgenerational epigenetic papers that discuss the mechanism of inheritance, and these would be represented in both the “mechanism” and 𠇎volution” category. However, as is evident from Figure 1 , the majority of the focus of epigenetic studies was on mechanism and disease states in approximately equal measure. Indeed, χ% of papers referencing epigenetics also mentioned either evolution and/or inheritance. Noteworthy is that while transgenerational epigenetics studies have revealed many instances of epigenetic inheritance of disease/pathologies (e.g., [3,27,28]), the epigenetic inheritance of mal-adaptive modified phenotypes receives little attention compared to the “here and now” of diseases that develop in an individual’s life span. These findings are not surprising, as even a quick examination of a sample of papers comprising the epigenetic literature reveals intensive discussion of mechanisms of epigenetic phenomena, especially as they relate to human health and disease. Additionally, to no one’s surprise, funding follows disease and its prevention and cure, which has greatly enabled the growth of epigenetic studies.
Radar diagram showing the relative distribution of publications drawn from the PubMed database (http://www.ncbi.nlm.nih.gov/pubmed/) that contain the search terms 𠇎pigenetic(s)” and one of five focus areas. The graphic to the right indicates a gradient between intragenerational and transgenerational epigenetics based on the percentage of epigenetic papers emerging from each area of study indicated in the radar diagram. Thus, epigenetic papers with the terms velopment and ageing” or 𠇍isease” are assumed to be more likely to be addressing intragenerational issues, such as evolution, while epigenetic papers mentioning 𠇎volution” or “inheritance” are viewed as more likely to be focusing on transgenerational epigenetic events. See the text for an additional discussion.
4.2. Epigenetics and Taxon
The survey next explored the taxonomic distribution of epigenetic papers using the secondary search terms (and their adjectives) of 𠇊nimals”, “plants”, 𠇏ungi”, “protists”, teria”, 𠇊rchaebacteria” and “viruses” . Approximately 60% of epigenetic papers contained the search term 𠇊nimal(s)”
10% contained “plant(s)” and near negligible numbers of epigenetic papers specifically mentioned any of the other major taxa ( Figure 2 A).
Radar diagram showing the relative distribution of publications on epigenetics drawn from the PubMed database (http://www.ncbi.nlm.nih.gov/pubmed/). (A) distribution of publications that contain the search terms 𠇎pigenetic(s)” and one of seven biological taxa (B) distribution of publications that contain the search terms 𠇎pigenetic(s)” and one of 12 biological fields.
4.3. Epigenetics and the Biological Field
The survey next considered epigenetic papers that included one of 12 major biological fields ( Figure 2 B). The vast majority (
95%) of epigenetic papers that even mentioned, if not actually discussed, a particular biological field was clustered in just six areas: chemistry/biochemistry, molecular biology, genetics, physiology, cellular biology or anatomy/morphology. Occurring at a very low frequency in the epigenetic literature were the fields of behavior (
2% of papers), taxonomy/systematics (1%𠄲%), evolution (a little above 1%) and, all being less than 0.5% of the epigenetic papers, development, ecology and evo-devo.
Combing the survey on biological fields and taxa reveals how some areas of epigenetics are almost completely unexplored. For example, combining 𠇎pigenetics” + “plant” + 𠇎vo-devo” yielded only two papers among the
50,000 epigenetics papers warehoused in PubMed. Similarly, 𠇎pigenetics” + “virus” + ology” yielded just three papers. Yet, as we will now turn to, the role of epigenetics in the biology of all of these taxa may be profound.
Principles of Natural Selection
There is an incredible variety of selective forces in the natural world, ranging from interspecies competition, to predator-prey dynamics, to sexual selection between the different genders. The defining characteristic of natural selection is that it is a force that allows some organisms to reproduce more than others. Natural selection does not always lead to the “right” answer, as some people tend to think.
Natural selection is an imperfect process. It cannot create new DNA spontaneously, or change the DNA it is given in meaningful ways. It can only slow or stop the reproduction of some DNA while allowing other DNA to persist. Every population has the opportunity to adapt, migrate to different conditions, or go extinct in the face of natural selection.
The process of natural selection screens the DNA it is given, with the minor mutations and recombination that occurs during replication, and simply does not let some DNA pass. Sometimes, the screen is random, as in a lighting strike killing a single tree. Other times, the screen is biased towards certain types of organisms, causing a selection to happen. This can be seen in the pine beetle invasion in North America. The pine beetles are being selected for because they are exploiting a rich food source. The pine trees, on the other hand, are being selected against for not having adequate defenses against the beetles.
Mechanism of Evolution: 4 Theories | Biology
The following points highlight the four main theories in mechanism of evolution. The theories are: 1. Lamarck’s Theory 2. Darwin’s Theory of Evolution 3. De Vries’ Theory 4. Modern Theory of Evolution.
1. Lamarck’s Theory:
Jean Baptiste Lamarck (1744-1829), a French naturalist, made several valuable contributions to biological science, including the coining of the term ‘biology’ and using the same in its true sense. He studied comparative anatomy and planned a tree of life for explaining the phylogenetic relationship among organisms.
He believed in the fundamental unity of living things and in a progressive development of forms and functions in all organisms. But the most important contribution of Lamarck —his theory of evolution—was framed in 1801 and published in the ‘Philosophic Zoologique’ in 1809, that is the year in which Charles Darwin was born.
The essence of the Lamarckian theory or La­marckism may be summarised as follows:
(1) Necessity in the organism may give rise to new structures or may lead to the disappearance of certain parts. Lamarck expressed this as the law of use and disuse. According to Lamarck an organ which is used extensively by the organism would enlarge and be­come more efficient, while disuse or lack of use of a particular organ would lead to its degene­ration and ultimate disappear­ance.
For example, the webbed toes of aquatic birds such as swans developed due to constant stretching of the skin at the bases of the toes in some ancestral form which lived on land. The necessity of the web of skin arose when the ancestors migrated into the water in search of food. This led to constant use and stretch­ing, thereby a change was induced and a paddle-like foot evolved.
Similarly, the ancestors of the snakes were lizard-like creatures with 1 two pairs of limbs and the modern snakes lost their limbs by constant disuse while passing through narrow crevices. Thus by differential use and disuse of various parts, an organism could change a good deal that is, the organism acquires certain new characteristics.
(2) The second part of Lamarck’s theory postulated that acquired traits induced by use or disuse of organs were transmitted to the offspring this is the law of inheritance of acquired characters. Lamarckism explains evolution of the modern giraffe in the following way.
There was a short-necked ancestral stock which used to feed on tree leaves. It stretched its neck further up, to reach higher levels, when the leaves lower down were finished. Due to constant stretching the neck length increased a little and his new trait was inherited by the offspring.
The latter in turn kept on stretching their necks and this was continued for many generations. Each successive generation would acquire the gains of the previous generation by inheritance, and would itself add a bit to the neck length. In the course of time, the long-necked modern giraffe evolved out of the short-necked ancestral form.
Criticism of Lamarckism:
The first part of Lamarck’s theory, that is, the law of use and disuse is acceptable. For example, moderate exercise taken regularly builds big muscles, or a limb put up on splints and not used for a long time undergoes atrophy. But the second part of Lamarckism, that is, inheritance of acquired characters, is not acceptable.
It implies that a man who has deve­loped large muscles by lifelong exercise will beget children with big muscles. Lamarckism was chiefly opposed by Weismann (1834- 1914) who postulated that germ cells are not affected materially by changes in the body cells.
In spite of the laborious research of neo-Lamarckists such as Guyer, Smith and Cope, Lamarckism is untenable. Acquired characters are phenotypic variations. They cannot affect the genes. As such they cannot be transmitted to the offspring.
2. Darwin’s Theory of Evolution:
The name of Charles Robert Darwin (1809-1882) is a proverb in the history of science. This illustrious grandson of Eras­mus Darwin was born in 1809 and his date of birth coincided with that of Abra­ham Lincoln. In his early life Darwin, like all other scientists of his time, believed in Lamarckism.
As a young man he joined the naval expeditionary ship ‘H.M.S. Beagle’ and undertook a circumglobal voyage for five long years. He spent his time in collecting numerous speci­mens of plants and animals from different parts of the world. After returning home Darwin spent 20 years in studying his collections.
At this time he was greatly in­fluenced by the publications of Lyell and Malthus. By studying Lyell’s ‘Principles of Geology’ Darwin learnt about the changing Jonas of the earth, and about the fossils which were known i: that time. The famous essay on population published by Malthus taught Darwin about overpopulation and consequent competition for food and shelter.
Having completed his study, Darwin was preparing his theory of natural selection for explaining the mechanism of organic evolution when he received an essay from a younger scientist, Alfred Russell Wallace (1823-1913), who was working independently on the flora and fauna of Malayan archipelago. To his amazement Darwin found that Wallace’s views on the origin of species coincided with his own theory.
The natural selection theory was first published as a paper under joint authorship in 1858. Two renowned scientists of that time, Lyell and Hooker, presented the paper at the meeting of the Linnean Society and Darwin was conspicuous by his absence. In the following year, that is in 1859, Darwin published his classical work in the form of a book—”On the origin of species by means of natural selection.”
Essence of Darwinism:
Darwin’s theory is based on intrin­sic analysis of facts in a scientific spirit by induction and deduction.
The following is the essence of Darwinism:
(1) Prodigality of Production:
The plants and animals have a tendency to increase in geometric progression, but the habitable space and the food supply remain constant. Darwin calculated that starting from a pair of elephants, the herd will increase to about 20,000,000 in 1000 years, and elephants are the slowest breeders producing 4 to 6 calves in their life-time. Such enormous prodigality in production results in struggle for existence.
(2) Struggle for Existence:
This means a keen competition amongst the living forms for food and shelter.
It operates in a three­fold way:
(a) Interspecific, that is, struggle in between different species of organisms,
(b) Intraspecific, that is, struggle between members of the same species, and
(c) Environmental, that is, struggle against the changes of the environment.
Darwin observed that no two living forms were exactly alike. Diversity tends to appear even among members belonging to the same species. Darwin paid particular attention to small, fluctuating and continuous variations which appeared randomly.
According to him these continuous variations help the organism to win the struggle for existence. Large, discontinuous variations, which appeared suddenly, were considered by Darwin as mere ‘sports of nature’, and therefore ignored.
(4) Survival of the Fittest:
The organisms possessing suitable variations which helped them to win the struggle for existence were better adapted to their environment. They survived and propagated their variations to the next generation. The others with unsuitable variations perished.
This is the most important deduction of Darwin. Natural selection is the process by which individuals possessing favourable variations enjoy a competitive advantage over the others.
They are better adapted to their environment, and therefore they survive in proportionately greater numbers and produce more offspring. The rest with disadvantageous variations fail to adapt properly to their environment and therefore eliminated by natural selection.
The favourable variations which are the cause of success are handed down to the offspring by inheritance. Thus the number of the favoured individuals increase rapidly, and if natural selection operates for a long time, those favourable variations which have attained the survival value are intensified successively from generation to generation, until the original ancestral forms are thoroughly changed into a new species.
For example, Darwinism explains the evolution of the modern giraffe in the following manner. The original ancestral forms were short-necked, leaf-eating animals. Darwin assumed that as a result of individual variation, some of them had slightly longer or shorter necks in comparison with the population’s average neck-length.
The longer-necked forms were better adapted to get at foliage’s situated a bit higher up. Consequently they were better fed than the shorter-necked fellows, and they produced proportionately greater numbers of offspring.
As a result of natural selection the proportion of the longer-necked population would be doubled in the next generation. This is repeated in successive generations until the entire population would be transformed into individuals with slightly longer necks.
Individual variation would occur in the new population and actual neck-lengths would vary more or less on either side of an average. Long necks would again be favoured in a second round of natural selection and then in successive rounds, until the modern giraffe with very long neck evolved out of the short-necked ancestral stock.
Criticism of Darwin’s Theory:
In spite of strong evidences and critical scanning of facts, Darwinism suffers from certain serious drawbacks.
A few objections to Darwinism are briefly discussed as follows:
(1) Variations were accepted by Darwin to be the chief tool in the process of evolution of new species, and he believed that small continuous variations of fluctuating type were inherited by the offspring. Unfortunately Darwin had no knowledge about the real cause of variation.
At this time the science of genetics was unknown, and the laws of inheritance were unexplored. Most of the fluctuat­ing variations considered by Darwin to be important factors in his theory of natural selection are not genotypic and as such they are not inherited.
(2) Darwin, like Lamarck, believed in the inheritance of acquired characters—a fact which is not proved by genetics.
(3) Darwin’s natural selection mainly operates in one direction, and often leads to over specialisation and ultimate extinction. The canine teeth of the sabre-toothed tiger and the antlers of the Irish elk increased progressively in size because the characteristics in both the cases were favoured by natural selection.
But ultimately, the structures became so large that instead of being helpful they became hindrance in the struggle for existence, and led to the extinction of the species.
(4) Natural selection theory fails to account for the degeneracy which is very often observed in the parasitic forms.
(5) The essence of Darwinian natural selection is the elimina­tion of the unsuitable forms. Hence it is better to name it as the ‘theory of natural rejection’.
(6) Darwin actually observed large, discontinuous variations or mutations to occur in nature. He rejected them as they occurred less frequently. But mutations are genotypic variations and they have now been recognised as important factors in the origin of new species.
In spite of its weakness Darwinism is still accepted as one of the important factors in evolution. Thanks to the untiring efforts of Thomas Henry Huxley (1825-1895), the great champion of natural selection, and others, such as August Weismann, the theory has been firmly established.
3. De Vries’ Theory:
The mutation theory was published in 1901 by the Dutch botanist, Hugo De Vries (1848-1935). His theory is mainly based on his experiments on a plant called evening primrose,
De Vries found that certain strikingly different forms appeared suddenly among a population of normal type of evening primrose. He called them mutants. A mutant is a variant which arises abruptly among normal forms. A mutant always breeds true, that is, it produces offspring like itself.
The term mutation or psaltation is applied to a sudden large change or discontinuous varia­tion in organisms, and this can be inherited. According to the mutation theory, mutations are the real cause for the evolution of a new species.
Numerous mutants may be produced in nature. They are then subjected to natural selec­tion .which determines the types that would survive. The mutants which survive in the struggle for existence are responsible for the origin of new species.
(1) Mutation often produces monsters which have no evolutionary significance.
(2) Mutations occur infrequently and they therefore cannot be regarded as the sole factor in evolution.
(3) Mutation theory accepts natural selection as the controlling agent in evolution.
4. Modern Theory of Evolution:
This is the product of recent researches in cytology, embryology, and genetics. In the opinion of modern scientists, the heritable characters of an individual rest upon particles of nucleoproteins or genes in the chromosomes of the gametes. Any variation in the characteristics of an individual, whether continuous or discontinuous, must come through changes in the genes.
Such changes that suit well with the environment are advantageous, and individuals possessing advantageous changes get the better chance of living and multiplying. This will continue for successive generation until a final form comes into existence, differing profusely from the ancestral type.
Natural selection acting as a screen leads to differential survival and differential reproduction. In the present outlook about the origin of species, Darwin’s struggle for existence may not be in the form of a compe­tition, but the selective value has been found to be more important in differential survival of different variations.
The modern theory explains the evolution of the giraffe in the following way: Every generation of the short-necked ancestral stock must have included a few mutant types, with shorter or longer necks than the average neck-length of the population.
The longer-necked individuals are in a more advantageous position. In the subsequent generation they will produce more longer-necked forms. This will go on through several generations in which changes in the gene would produce mutants, and natural selection acting as a screen would again and again eliminate the short-necked individuals, until the appearance of the modern giraffe with very long neck.
This modern theory is known as the synthetic theory. Several investigators of the synthetic school, such as Haldane, Ford, Waddington, Miller, Dobzhansky, and others have contributed their bit in its shaping. It is nothing but a completely re-modelled natural selection theory minus its weaknesses.
What is Natural Selection
Natural selection is the main process which drives evolution by aiding organisms to survive and produce more offspring through adapting more to their environment. Mutations, gene flow, and genetic drift also drive evolution. The grand idea about evolution was first fully expounded by Charles Darwin. Variation, inheritance, high rate of population growth, and differential survival and reproduction are the four components of Darwin’s process of natural selection. Genetic variations can be observed among individuals within the same population due to mutations, gene flow, and genetic drift. All individuals do not reproduce in their full potential. Thus, differential reproduction allows the inheritance of a set of selected characters to the offspring. On that account, the phenotypes that fit the environment best may accumulate in the offspring.
Figure 1: Light and dark color moths
The most well-known evidence of natural selection is the adaptation of moths under the effect of the industrial revolution. Soot and other industrial wastes darkened the tree trunks. The lichens were killed as well by pollution. Thus, the light color morph of the peppered moth became less common due to the selective predation of birds due to the camouflage coloration in the moth. The dark morph becomes more abundant. The light and dark color moths on a tree truck are shown in figure 1.
Problem 3: Step-by-Step Random Mutations Cannot Generate the Genetic Information Needed for Irreducible Complexity
Editor’s note: This is Part 3 of a 10-part series based upon Casey Luskin’s chapter, “The Top Ten Scientific Problems with Biological and Chemical Evolution,” in the volume More than Myth, edited by Paul Brown and Robert Stackpole (Chartwell Press, 2014). The full chapter can be found online here. Other individual installments can be found here: Problem 1, Problem 2, Problem 4, Problem 5, Problem 6, Problem 7, Problem 8, Problem 9, Problem 10.
According to evolutionary biologists, once life got started, Darwinian evolution took over and eventually produced the grand diversity we observe today. Under the standard view, a process of random mutation and natural selection built life’s vast complexity one small mutational step at a time. All of life’s complex features, of course, are thought to be encoded in the DNA of living organisms. Building new features thus requires generating new information in the genetic code of DNA. Can the necessary information be generated in the undirected, step-by-step manner required by Darwin’s theory?
Most everyone agrees that Darwinian evolution tends to work well when each small step along an evolutionary pathway provides some survival advantage. Darwin-critic Michael Behe notes that “if only one mutation is needed to confer some ability then Darwinian evolution has little problem finding it.” 24 However, when multiple mutations must be present simultaneously to gain a functional advantage, Darwinian evolution gets stuck. As Behe explains, “If more than one [mutation] is needed, the probability of getting all the right ones grows exponentially worse.” 25
Behe, a professor of biochemistry at Lehigh University, coined the term “irreducible complexity” to describe systems which require many parts — and thus many mutations — to be present — all at once — before providing any survival advantage to the organism. According to Behe, such systems cannot evolve in the step-by-step fashion required by Darwinian evolution. As a result, he maintains that random mutation and unguided natural selection cannot generate the genetic information required to produce irreducibly complex structures. Too many simultaneous mutations would be required — an event which is highly unlikely to occur.
Observation of this problem is not limited to Darwin-critics. A paper by a prominent evolutionary biologist in the prestigious journal Proceedings of the U.S. National Academy of Science. acknowledges that “simultaneous emergence of all components of a system is implausible.” 26 Likewise, University of Chicago evolutionary biologist Jerry Coyne — a staunch defender of Darwinism — admits that “natural selection cannot build any feature in which intermediate steps do not confer a net benefit on the organism.” 27 Even Darwin intuitively recognized this problem, as he wrote in Origin of Species:
If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. 28
Evolutionary scientists like Darwin and Coyne claim they know of no real-world case where Darwinian selection gets blocked in this manner. But they would agree, at least in principle, that there are theoretical limits to what Darwinian evolution can accomplish: If a feature cannot be built by “numerous, successive, slight modifications,” and if “intermediate steps do not confer a net benefit on the organism,” then Darwinian evolution will “absolutely break down.”
The problems are real. Modern biology continues to uncover more and more examples where biological complexity seems to outstrip the information-generative capacity of Darwinian evolution.
In his book Darwin’s Black Box, Michael Behe discusses molecular machines which require multiple parts to be present before they could function and confer any advantage on the organism. Behe’s most famous example is the bacterial flagellum — a micromolecular rotary-engine, functioning like an outboard motor on bacteria to propel it through liquid medium to find food. In this regard, flagella have a basic design that is highly similar to some motors made by humans containing many parts that are familiar to engineers, including a rotor, a stator, a u-joint, a propeller, a brake, and a clutch. As one molecular biologist writes in the journal Cell, “[m]ore so than other motors, the flagellum resembles a machine designed by a human.” 29 However the energetic efficiency of these machines outperforms anything produced by humans: the same paper found that the efficiency of the bacterial flagellum “could be
There are various types of flagella, but all use certain basic components. As one paper in Nature Reviews Microbiology acknowledges, “all (bacterial) flagella share a conserved core set of proteins” since “Three modular molecular devices are at the heart of the bacterial flagellum: the rotor-stator that powers flagellar rotation, the chemotaxis apparatus that mediates changes in the direction of motion and the T3SS that mediates export of the axial components of the flagellum.” 31 As this might suggest, the flagellum is irreducibly complex. Genetic knockout experiments have shown that it fails to assemble or function properly if any one of its approximately 35 genes are missing. 32 In this all-or-nothing game, mutations cannot produce the complexity needed to provide a functional flagellar rotary engine one incremental step at a time, and the odds are too daunting for it to assemble in one great leap. Indeed, the aforementioned Nature Reviews Microbiology paper admitted that “the flagellar research community has scarcely begun to consider how these systems have evolved.” 33
Yet the flagellum is just one example of thousands of known molecular machines in biology. One individual research project reported the discovery of over 250 new molecular machines in yeast alone. 34 The former president of the U.S. National Academy of Sciences, Bruce Alberts, wrote an article in the journal Cell praising the “speed,” “elegance,” “sophistication,” and “highly organized activity” of these “remarkable” and “marvelous” molecular machines. He explained what inspired those words: “Why do we call the large protein assemblies that underlie cell function protein machines? Precisely because, like machines invented by humans to deal efficiently with the macroscopic world, these protein assemblies contain highly coordinated moving parts.” 35 Biochemists like Behe and others believe that with all of their coordinated interacting parts, many of these machines could not have evolved in a step-by-step Darwinian fashion.
But it’s not just multi-part machines which are beyond reach of Darwinian evolution. The protein-parts themselves which build these machines would also require multiple simultaneous mutations in order to arise.
Research Challenges the Darwinian Mechanism
In 2000 and 2004, protein scientist Douglas Axe published experimental research in the Journal of Molecular Biology on mutational sensitivity tests he performed on enzymes in bacteria. 36 Enzymes are long chains of amino acids which fold into a specific, stable, three-dimensional shape in order to function. Mutational sensitivity experiments begin by mutating the amino acid sequences of those proteins, and then testing the mutant proteins to determine whether they can still fold into a stable shape, and function properly. Axe’s research found that amino acid sequences which yield stable, functional protein folds may be as rare as 1 in 10 74 sequences, suggesting that the vast majority of amino acid sequences will not produce stable proteins, and thus could not function in living organisms.
Because of this extreme rarity of functional protein sequences, it would be very difficult for random mutations to take a protein with one type of fold, and evolve it into another, without going through some non-functional stage. Rather than evolving by “numerous, successive, slight modifications,” many changes would need to occur simultaneously to “find” the rare and unlikely amino acid sequences that yield functional proteins. To put the matter in perspective, Axe’s results suggest that the odds of blind and unguided Darwinian processes producing a functional protein fold are less than the odds of someone closing his eyes and firing an arrow into the Milky Way galaxy, and hitting one pre-selected atom. 37
Proteins commonly interact with other molecules through a “hand-in-glove” fit, but these interactions often require multiple amino acids to be ‘just right’ before they occur. In 2004, Behe, along with University of Pittsburgh physicist David Snoke, simulated the Darwinian evolution of such protein-protein interactions. Behe and Snoke’s calculations found that for multicellular organisms, evolving a simple protein-protein interaction which required two or more mutations in order to function would probably require more organisms and generations than would be available over the entire history of the Earth. They concluded that “the mechanism of gene duplication and point mutation alone would be ineffective…because few multicellular species reach the required population sizes.” 38
Four years later during an attempt to refute Behe’s arguments, Cornell biologists Rick Durrett and Deena Schmidt ended up begrudgingly confirming he was basically correct. After calculating the likelihood of two simultaneous mutations arising via Darwinian evolution in a population of humans, they found that such an event “would take > 100 million years.” Given that humans diverged from their supposed common ancestor with chimpanzees only 6 million years ago, they granted that such mutational events are “very unlikely to occur on a reasonable timescale.” 39
Now a defender of Darwinism might reply that these calculations measured the power of the Darwinian mechanism only within multicellular organisms where it is less efficient because these more complex organisms have smaller population sizes and longer generation times than single-celled prokaryotic organisms like bacteria. Darwinian evolution, the Darwinian notes, might have a better shot when operating in organisms like bacteria, which reproduce more rapidly and have much larger population sizes. Scientists skeptical of Darwinian evolution are aware of this objection, and have found that even within more-quickly evolving organisms like bacteria, Darwinian evolution faces great limits.
In 2010, Douglas Axe published evidence indicating that despite high mutation rates and generous assumptions favoring a Darwinian process, molecular adaptations requiring more than six mutations before yielding any advantage would be extremely unlikely to arise in the history of the Earth.
The following year, Axe published research with developmental biologist Ann Gauger regarding experiments to convert one bacterial enzyme into another closely related enzyme — the kind of conversion that evolutionists claim can easily happen. For this case they found that the conversion would require a minimum of at least seven simultaneous changes, 40 exceeding the six-mutation-limit which Axe had previously established as a boundary of what Darwinian evolution is likely to accomplish in bacteria. Because this conversion is thought to be relatively simple, it suggests that more complex biological features would require more than six simultaneous mutations to give some new functional advantage.
In other experiments led by Gauger and biologist Ralph Seelke of the University of Wisconsin, Superior, their research team broke a gene in the bacterium E. coli required for synthesizing the amino acid tryptophan. When the bacteria’s genome was broken in just one place, random mutations were capable of “fixing” the gene. But even when only two mutations were required to restore function, Darwinian evolutionseemed to get stuck, with an inability to regain full function. 41
These kind of results consistently suggest that the information required for proteins and enzymes to function is too great to be generated by Darwinian processes on any reasonable evolutionary timescale.
Darwin Skeptics Abound
Drs. Axe, Gauger, and Seelke are by no means the only scientists to observe the rarity of amino acid sequences that yield functional proteins. A leading college-level biology textbook states that “even a slight change in primary structure can affect a protein’s conformation and ability to function.” 42 Likewise, evolutionary biologist David S. Goodsell writes:
[O]nly a small fraction of the possible combinations of amino acids will fold spontaneously into a stable structure. If you make a protein with a random sequence of amino acids, chances are that it will only form a gooey tangle when placed in water. 43
Goodsell goes on to assert that “cells have perfected the sequences of amino acids over many years of evolutionary selection.” But if functional protein sequences are rare, then it is likely that natural selection will be unable to take proteins from one functional genetic sequence to another without getting stuck in some maladaptive or non-beneficial intermediate stage.
The late biologist Lynn Margulis, a well-respected member of the National Academy of Sciences until her death in 2011, once said “new mutations don’t create new species they create offspring that are impaired.” 44 She further explained in a 2011 interview:
[N]eo-Darwinists say that new species emerge when mutations occur and modify an organism. I was taught over and over again that the accumulation of random mutations led to evolutionary change-led to new species. I believed it until I looked for evidence. 45
Similarly, past president of the French Academy of Sciences, Pierre-Paul Grasse, contended that “[m]utations have a very limited ‘constructive capacity'” because “[n]o matter how numerous they may be, mutations do not produce any kind of evolution.” 46