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15.2: Cell Cycle and Cell Division - Biology

15.2: Cell Cycle and Cell Division - Biology


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So Many Cells!

The baby in Figure (PageIndex{1}) has a lot of growing to do before they are as big as their mom. Most of their growth will be the result of cell division. By the time the baby is an adult, their body will consist of trillions of cells. Cell division is just one of the stages that all cells go through during their life. This includes cells that are harmful, such as cancer cells. Cancer cells divide more often than normal cells and grow out of control. In fact, this is how cancer cells cause illness. In this concept, you will read about how cells divide, what other stages cells go through, and what causes cancer cells to divide out of control and harm the body.

The Cell Cycle

Cell division is the process in which one cell, called the parent cell, divides to form two new cells, referred to as daughter cells. How this happens depends on whether the cell is prokaryotic or eukaryotic. Cell division is simpler in prokaryotes than eukaryotes because prokaryotic cells themselves are simpler. Prokaryotic cells have a single circular chromosome, no nucleus, and few other organelles. Eukaryotic cells, in contrast, have multiple chromosomes contained within a nucleus and many other organelles. All of these cell parts must be duplicated and then separated when the cell divides. Cell division is just one of several stages that a cell goes through during its lifetime. The cell cycle is a repeating series of events that include growth, DNA synthesis, and cell division. The cell cycle in prokaryotes is quite simple: the cell grows, its DNA replicates, and the cell divides. This form of division in prokaryotes is called asexual reproduction. In eukaryotes, the cell cycle is more complicated.

Eukaryotic Cell Cycle

Figure (PageIndex{2}) represents the cell cycle of a eukaryotic cell. As you can see, the eukaryotic cell cycle has several phases. The mitotic phase (M) includes both mitosis and cytokinesis. This is when the nucleus and then the cytoplasm divide. The other three phases (G1, S, and G2) are generally grouped together as interphase. During interphase, the cell grows, performs routine life processes, and prepares to divide. These phases are discussed below.

Interphase

The Interphase of the eukaryotic cell cycle can be subdivided into the following phases (Figure (PageIndex{2})).

  • Growth Phase 1 (G1): The cell spends most of its life in the first gap (sometimes referred to as growth) phase, G1. During this phase, a cell undergoes rapid growth and performs its routine functions. During this phase, the biosynthetic and metabolic activities of the cell occur at a high rate. The synthesis of amino acids and hundreds of thousands or millions of proteins that are required by the cell occurs during this phase. Proteins produced include those needed for DNA replication. If a cell is not dividing, the cell enters the G0 phase from this phase.
  • G0 phase: The G0 phase is a resting phase where the cell has left the cycle and has stopped dividing. Non-dividing cells in multicellular eukaryotic organisms enter G0 from G1. These cells may remain in G0 for long periods of time, even indefinitely, such as with neurons. Cells that are completely differentiated may also enter G0. Some cells stop dividing when issues of sustainability or viability of their daughter cells arise, such as with DNA damage or degradation, a process called cellular senescence. Cellular senescence occurs when normal diploid cells lose the ability to divide, normally after about 50 cell divisions.
  • Synthesis Phase (S): Dividing cells enter the Synthesis (S) phase from G1. For two genetically identical daughter cells to be formed, the cell’s DNA must be copied through DNA replication. When the DNA is replicated, both strands of the double helix are used as templates to produce two new complementary strands. These new strands then hydrogen bond to the template strands and two double helices form. During this phase, the amount of DNA in the cell has effectively doubled, though the cell remains in a diploid state.
  • Growth Phase 2 (G2): The second gap (growth) (G2) phase is a shortened growth period in which many organelles are reproduced or manufactured. Parts necessary for mitosis and cell division are made during G2, including microtubules used in the mitotic spindle.

Mitotic Phase

Before a eukaryotic cell divides, all the DNA in the cell’s multiple chromosomes is replicated. Its organelles are also duplicated. This happens in the interphase. Then, when the cell divides (mitotic phase), it occurs in two major steps, called mitosis and cytokinesis, both of which are described in greater detail in the concept Mitotic Phase: Mitosis and Cytokinesis.

  • The first step in the mitotic phase of a eukaryotic cell is mitosis, a multi-phase process in which the nucleus of the cell divides. During mitosis, the nuclear envelope (membrane) breaks down and later reforms. The chromosomes are also sorted and separated to ensure that each daughter cell receives a complete set of chromosomes.
  • The second major step is cytokinesis. This step, which occurs in prokaryotic cells as well, is when the cytoplasm divides and two daughter cells form.
Table (PageIndex{2}): Cell Cycle Summary

State

Name

Description

Quiescent Senescent

Resting phase (G0)

A resting phase where the cell has left the cycle and has stopped dividing.

Interphase

1st growth phase (G1)

Synthesis phase (S)

2ndgrowth phase (G2)

Cells increase in size in G1. Cells perform their normal activities.

DNA replication occurs during this phase.

The cell will continue to grow and many organelles will divide during their phase.

Cell division

Mitosis (M)

Cell growth stops at this stage. Mitosis divides the nucleus into two nuclei, followed by cytokinesis which divides the cytoplasm. Two genetically identical daughter cells result.

Control of the Cell Cycle

If the cell cycle occurred without regulation, cells might go from one phase to the next before they were ready. What controls the cell cycle? How does the cell know when to grow, synthesize DNA, and divide? The cell cycle is controlled mainly by regulatory proteins. These proteins control the cycle by signaling the cell to either start or delay the next phase of the cycle. They ensure that the cell completes the previous phase before moving on. Regulatory proteins control the cell cycle at key checkpoints, which are shown in Figure (PageIndex{3}). There are a number of main checkpoints:

  1. The G1 checkpoint: just before entry into the S phase, makes the key decision of whether the cell big enough to divide. If the cell is not big enough, it goes into the resting period (G0)
  2. DNA synthesis Checkpoint: The S checkpoint determines if the DNA has been replicated properly.
  3. The mitosis checkpoint: This checkpoint ensures that all the chromosomes are properly aligned before the cell is allowed to divide.

Cancer and the Cell Cycle

Cancer is a disease that occurs when the cell cycle is no longer regulated. This happens because a cell’s DNA becomes damaged. This results in mutations in the genes that regulate the cell cycle. Damage can occur due to exposure to hazards such as radiation or toxic chemicals. Cancerous cells generally divide much faster than normal cells. They may form a mass of abnormal cells called a tumor (see Figure (PageIndex{4})). The rapidly dividing cells take up nutrients and space that normal cells need. This can damage tissues and organs and eventually lead to death. When uncontrolled cell division happens in the bone marrow, abnormal and nonfunctional blood cells are produced because the division is happening before the cell is ready for division. In these types of cancer, there is not any evident tumor.

Feature: Human Biology in the News

Henrietta Lacks sought treatment for her cancer at Johns Hopkins University Hospital at a time when researchers were trying to grow human cells in the lab for medical testing. Despite many attempts, the cells always died before they had undergone many cell divisions. Mrs. Lacks's doctor took a small sample of cells from her tumor without her knowledge and gave them to a Johns Hopkins researcher, who tried to grow them on a culture plate. For the first time in history, human cells grown on a culture plate kept dividing...and dividing and dividing and dividing. Copies of Henrietta's Lacks cells — called HeLa cells for her name — are still alive today. In fact, there are currently many billions of HeLa cells in laboratories around the world!

Why Henrietta Lacks' cells lived on when other human cells did not is still something of a mystery, but they are clearly extremely hardy and resilient cells. By 1953, when researchers learned of their ability to keep dividing indefinitely, factories were set up to start producing the cells commercially on a large scale for medical research. Since then, HeLa cells have been used in thousands of studies and have made possible hundreds of medical advances. For example, Jonas Salk used the cells in the early 1950s to test his polio vaccine. Over the decades since then, HeLa cells have been used to make important discoveries in the study of cancer, AIDS, and many other diseases. The cells were even sent to space on early space missions to learn how human cells respond to zero gravity. HeLa cells were also the first human cells ever cloned, and their genes were some of the first ever mapped. It is almost impossible to overestimate the profound importance of HeLa cells to human biology and medicine.

You would think that Henrietta Lacks' name would be well known in medical history for her unparalleled contributions to biomedical research. However, until 2010, her story was virtually unknown. That year, a science writer named Rebecca Skloot published a nonfiction book about Henrietta Lacks, named The Immortal Life of Henrietta Lacks. Based on a decade of research, the book is riveting, and it became an almost instantaneous best seller. As of 2016, Oprah Winfrey and collaborators planned to make a movie based on the book, and in recent years, numerous articles about Henrietta Lacks have appeared in the press.

Ironically, Henrietta herself never knew her cells had been taken, and neither did her family. While her cells were making a lot of money and building scientific careers, her children were living in poverty, too poor to afford medical insurance. The story of Henrietta Lacks and her immortal cells raises ethical issues about human tissues and who controls them in biomedical research. However, there is no question that Henrietta Lacks deserves far more recognition for her contribution to the advancement of science and medicine.

Review

  1. What are the two main phases of the cell cycle in a eukaryotic cell?
  2. Describe the three phases of interphase in a eukaryotic cell.
  3. Explain how the cell cycle is controlled.
  4. How is cancer-related to the cell cycle?
  5. What are the two major steps of cell division in a eukaryotic cell?
  6. In which phase of the eukaryotic cell cycle do cells typically spend most of their lives?
  7. Which phases of the cell cycle will have cells with twice the amount of DNA? Explain your answer.
  8. If there is damage to a gene that encodes for a cell cycle regulatory protein, what do you think might happen? Explain your answer.
  9. True or False. Cells go into G0 if they do not pass the G1 checkpoint.
  10. In which phase within interphase does the cell make final preparations to divide?
    1. Mitosis
    2. Cytokinesis
    3. G2
    4. S
  11. What were scientists trying to do when they took tumor cells from Henrietta Lacks? Why did they specifically use tumor cells to try to achieve their goal?

Explore More

The video below discusses the cell cycle and how it relates to cancer.


39 6.2 The Cell Cycle

The cell cycle is an ordered series of events involving cell growth and cell division that produces two new daughter cells. Cells on the path to cell division proceed through a series of precisely timed and carefully regulated stages of growth, DNA replication, and division that produce two genetically identical cells. The cell cycle has two major phases: interphase and the mitotic phase (Figure 6.3). During interphase, the cell grows and DNA is replicated. During the mitotic phase, the replicated DNA and cytoplasmic contents are separated and the cell divides.

Figure 6.3 A cell moves through a series of phases in an orderly manner. During interphase, G1 involves cell growth and protein synthesis, the S phase involves DNA replication and the replication of the centrosome, and G2 involves further growth and protein synthesis. The mitotic phase follows interphase. Mitosis is nuclear division during which duplicated chromosomes are segregated and distributed into daughter nuclei. Usually the cell will divide after mitosis in a process called cytokinesis in which the cytoplasm is divided and two daughter cells are formed.


Concept in Action

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To make two daughter cells, the contents of the nucleus and the cytoplasm must be divided. The mitotic phase is a multistep process during which the duplicated chromosomes are aligned, separated, and moved to opposite poles of the cell, and then the cell is divided into two new identical daughter cells. The first portion of the mitotic phase, mitosis, is composed of five stages, which accomplish nuclear division. The second portion of the mitotic phase, called cytokinesis, is the physical separation of the cytoplasmic components into two daughter cells.

Mitosis is divided into a series of phases—prophase, prometaphase, metaphase, anaphase, and telophase—that result in the division of the cell nucleus (Figure 6.4).

Figure 6.4 Animal cell mitosis is divided into five stages—prophase, prometaphase, metaphase, anaphase, and telophase—visualized here by light microscopy with fluorescence. Mitosis is usually accompanied by cytokinesis, shown here by a transmission electron microscope. (credit “diagrams”: modification of work by Mariana Ruiz Villareal credit “mitosis micrographs”: modification of work by Roy van Heesbeen credit “cytokinesis micrograph”: modification of work by the Wadsworth Center, NY State Department of Health donated to the Wikimedia foundation scale-bar data from Matt Russell)

Which of the following is the correct order of events in mitosis?

  1. Sister chromatids line up at the metaphase plate. The kinetochore becomes attached to the mitotic spindle. The nucleus re-forms and the cell divides. The sister chromatids separate.
  2. The kinetochore becomes attached to the mitotic spindle. The sister chromatids separate. Sister chromatids line up at the metaphase plate. The nucleus re-forms and the cell divides.
  3. The kinetochore becomes attached to metaphase plate. Sister chromatids line up at the metaphase plate. The kinetochore breaks down and the sister chromatids separate. The nucleus re-forms and the cell divides.
  4. The kinetochore becomes attached to the mitotic spindle. Sister chromatids line up at the metaphase plate. The kinetochore breaks apart and the sister chromatids separate. The nucleus re-forms and the cell divides.

During prophase, the “first phase,” several events must occur to provide access to the chromosomes in the nucleus. The nuclear envelope starts to break into small vesicles, and the Golgi apparatus and endoplasmic reticulum fragment and disperse to the periphery of the cell. The nucleolus disappears. The centrosomes begin to move to opposite poles of the cell. The microtubules that form the basis of the mitotic spindle extend between the centrosomes, pushing them farther apart as the microtubule fibers lengthen. The sister chromatids begin to coil more tightly and become visible under a light microscope.

During prometaphase, many processes that were begun in prophase continue to advance and culminate in the formation of a connection between the chromosomes and cytoskeleton. The remnants of the nuclear envelope disappear. The mitotic spindle continues to develop as more microtubules assemble and stretch across the length of the former nuclear area. Chromosomes become more condensed and visually discrete. Each sister chromatid attaches to spindle microtubules at the centromere via a protein complex called the kinetochore.

During metaphase, all of the chromosomes are aligned in a plane called the metaphase plate, or the equatorial plane, midway between the two poles of the cell. The sister chromatids are still tightly attached to each other. At this time, the chromosomes are maximally condensed.

During anaphase, the sister chromatids at the equatorial plane are split apart at the centromere. Each chromatid, now called a chromosome, is pulled rapidly toward the centrosome to which its microtubule was attached. The cell becomes visibly elongated as the non-kinetochore microtubules slide against each other at the metaphase plate where they overlap.

During telophase, all of the events that set up the duplicated chromosomes for mitosis during the first three phases are reversed. The chromosomes reach the opposite poles and begin to decondense (unravel). The mitotic spindles are broken down into monomers that will be used to assemble cytoskeleton components for each daughter cell. Nuclear envelopes form around chromosomes.


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      4. Advances in Biological Technologies

      4.1. Medical Imaging Technologies

      4.1.1.1. Can easily penetrate materials such as skin and tissue but cannot easily penetrate metals and bone.

      4.1.1.1.1. Can be used to check for cancer and to diagnose problems in the cardiovascular and respiratory systems.

      4.1.1.1.2. Used by dentists to check for cavities in your teeth.

      4.1.1.1.3. Mammographs uses x-rays to check breast tissue for the presence of cancer.

      4.1.2.1. Uses a continuous beam of x-rays to produce images that show the movements of organs, such s the stomach, intestine, and colon, in the body.

      4.1.2.1.1. Used to study the blood vessels of the heart and the brain.

      4.1.3.1. During radiotherapy, a beam of x-rays is directed at a tumour so that there is minimal damage to healthy normal cells.

      4.1.3.1.1. Damage the DNA snd either kill the cancer cells or prevent them from multiplying

      4.1.4.1. Ultrasound imaging uses high-frequency sound waves to produce images of body tissues and organs.

      4.1.4.1.1. Used to study soft tissues and major organs in the body.

      4.1.4.1.2. Cannot penetrate bone

      4.1.5. Computed Assisted Tomography

      4.1.5.1. CAT involves using x-ray equipment to form a three-dimensional image from a series of images taken at different angles

      4.1.5.1.1. Frequently used t diagnose cancer, abnormalities of the skeletal system, and vascular diseases.

      4.1.6. Magnetic Resonance Imaging

      4.1.6.1. MRI uses powerful magnets and radiowaves to produce detailed images of the body.

      4.1.6.1.1. Useful for imaging the structure and function of the brain, heart and liver, soft tissues, and the inside of bones.


      Total stomach 34 1 2 0 3 Ovarian Tissue Sample 1

      19 0 0 1 0

      18 0 1 2 0

      Table 2: Record your data for the number of cells in each stage of the cell cycle observed in cancerous tissues.

      Tissue Type # Cells in Interphase

      Telophas e Lung Tissue Sample 1

      15 1 3 0 1

      16 0 2 1 1

      Total lung 31 1 5 1 2 Stomach Tissue Sample 1

      14 2 1 1 2

      13 2 2 2 1

      27 4 3 3 3

      12 2 1 2 3

      11 2 2 3 2

      23 4 3 5 5

      Table 3: Use the data in Table 1 to calculate the Mitotic Index (average % cells dividing) for each normal tissue type.

      Tissue Type Avg. % cells at rest Mitotic Index Lung - normal 15.2% 5% Stomach - normal 13.6% 15% Ovary - normal 15.17% 9.756%


      MATERIALS AND METHODS

      Construction of a Germ-line–targeted ER Marker

      The signal peptidase SP12 (C34B2.10) has been used as an ER marker in somatic C. elegans tissues (Rolls et al., 2002). N2 genomic DNA of the C34B2.10 gene coding for an ER resident protein signal peptidase (SP12) was amplified by PCR. The resulting product lacking the first methionine of the coding sequence was cloned into pENTR/D Gateway vector (Invitrogen, Carlsbad, CA). The vector pID3.01 was a generous gift from G. Seydoux. It contains the unc-119 rescuing sequence, EGFP cDNA under the germline-specific pie-1 promoter and a Gateway cassette allowing creation of N-terminal fusions with GFP. SP12 was placed into this vector by the LR Clonase (Invitrogen) reaction between pENTR/D donor and pID3.01 acceptor plasmids.

      Biolistic Transformation

      Transformation of worms with the vector containing the GFP::SP12 fusion sequence was performed as described by Praitis et al. (2001). Basically, the plasmid described above was coated onto 1-μm gold beads (Bio-Rad, Hercules, CA). unc-119 mutant worms were then bombarded with these coated beads using the Bio-Rad PDS-1000/He Particle Delivery System (Bio-Rad). After bombardment, worms were permitted to grow on 100-mm NGM plates for at least 2 wk. Worms that were rescued by the plasmid (phenotypically wild-type) were examined for GFP expression and those lines expressing GFP were maintained for experimental use. To assist with the timing analysis in utero, one of these lines was crossed with the H2B::GFP-expressing line, AZ212 (Praitis et al., 2001).

      Immunocytochemistry

      Mouse monoclonal anti-HDEL antibodies were kindly provided by S. Munro (MRC, Cambridge, United Kingdom). Immunocytochemistry was performed essentially as described (Pichler et al., 2000). Briefly, embryos from the SP12::GFP-expressing strain, immobilized on poly-lysine–coated slides, were freeze-cracked and fixed with 3.7% formaldehyde, 75% methanol, 0.5× phosphate-buffered saline for 15 min at –20°C followed by 15 min in absolute methanol. The slides were then rehydrated in PBST. Blocking was performed in PBST containing 5% bovine serum albumin. HDEL antibodies were diluted 1:20 in PBST and incubated with the embryos at 4°C overnight. Secondary CY3-conjugated antibodies (Jackson ImmunoResearch Laboratories, West Grove, PA) were diluted 1:300 and added for 1 h at RT. This treatment did not reduce the fluorescence of SP12::GFP substantially.

      PCR amplified fragments of the C. elegans genomic DNA corresponding to exons of the genes of interest were used to produce double-stranded RNA for microinjection into the gonad or intestine as described by Fire et al. (1998). Typically 18–25 L4 and young hermaphrodites of the SP12::GFP strain were injected with the appropriate dsRNA and analyzed 18–24 h postinjection. Usually, the concentration of injected dsRNA was 1 μg/μl. For the genes where RNAi resulted in sterility, we reduced the dsRNA concentration 3–8-fold. The brood size of these worms was still very low, and the embryonic lethality approached 100%.

      The following C. elegans putative orthologues of the mammalian and yeast genes were subjected to RNAi cdk-1 Cdc48/p97: C06A1.1 (78%), C41C4.8 (79%), and K04G2.3 (34%) (identity to human orthologues is indicated) p47: Y94H6A.9 BiP/Kar2: hsp-3 hsp-4 hsp-1 Jem1: dnj-10 rab-1 NSF/Sec18: nsf-1 Sar1: inx-9 (ZK792.3) sec-23 arf-1 nmy-2. RNAi against α-tubulin (tba-2) was performed using the feeding method described by Kamath and Ahringer (2003).

      Multiphoton and Confocal Microscopy

      Confocal time-lapse image series were acquired with a Leica TCS SP2 confocal laser scanning microscope system (Deerfield, IL). The laser intensity, scanning speed and time intervals were adjusted empirically not to affect the wild-type embryo viability for at least 1 h of imaging time. Embryos from the dissected worms were mounted on agarose pads in egg salts buffer. For the in utero imaging the worms were immobilized with 12 mM levamizole. Images were processed with either Leica LCS software or Adobe Photoshop 6.0 (San Jose, CA). Live oocytes and embryos were imaged using a multiphoton excitation-based optical workstation (Wokosin et al., 2003) that included a Nikon Eclipse (Nikon, Melville, NY) inverted microscope, a 100× oil immersion lens (1.3 NA), and a Spectra Physics (Spectra Physics, Mountain View, CA) titanium sapphire laser set at a wavelength of 900 nm. The scanning and image collection were controlled via the Bio-Rad Lasersharp software (Bio-Rad, Hercules, CA). Imaging intervals ranged from 2.22 to 8 s, depending on image size and scan rate. Embryos and worms were mounted as described for confocal imaging.

      For the quantification of the ER asymmetry during the first zygotic division, we took confocal images of the embryos during pronuclear rotation and centration. ER patches ≥1.5 μm in diameter in direct vicinity of the cortex were counted.

      For the 3D reconstruction from confocal images, Z-stacks of confocal images were analyzed for two typical stages: interphase and the onset of mitosis. Any continuous ER structures, along with the nuclear envelope were manually traced. Each plane was assigned a distinct color. The outlines were then superimposed according to their Z-stack order. The 3D reconstruction is an angle view rotated 45° along the X axis. The spacing between Z-stacks in this reconstruction was set in scale with the actual spacing of confocal images.

      Preparation of C. elegans Embryos for EM and Image Analysis

      Whole young adult worms containing embryos were prepared by high-pressure freezing followed by freeze substitution as described by McDonald (1999). The substitution was carried out in two stages: 1) incubating in the primary medium for 68 h at –90°C and then warming to –60°C, and 2) rinsing and replacing with the secondary medium for an additional 26 h as the samples were slowly warmed to 0°C. The primary medium was 1% glutaraldehyde dissolved in 98% acetone/2% water. The secondary medium was 2% osmium tetroxide dissolved in 98% acetone/2% water (Walther and Ziegler, 2002). Serial longitudinal sections 65 nm thick were collected and stained with saturated aqueous uranyl acetate followed by 0.4% lead citrate. Imaging was performed on a Phillips CM 120 (FEI, Hillsboro, OR) at 80 kV.

      Digital images captured on Soft Imaging Systems (Lakewood, CO) CCD camera and software, were automatically stitched together using the “Multiple Image Alignment” tool. Images were imported to Photoshop (Adobe Systems) and RER was highlighted using the brush tool on a second image layer. Sequential layers with different colored highlights were then pasted to a new image and aligned as closely as possible to each other using the x,y translation and rotate tools.

      Drug Treatment

      Embryos expressing the SP12::GFP fusion protein were treated with pharmacological compounds that interfere with cytoskeletal dynamics using laser ablation basically as previously described (Skop et al., 2001 Wokosin et al., 2003). Briefly, the embryos were sensitized in 1 mg/ml Trypan Blue in egg salts for ∼30 s on a coverslip. The Trypan Blue solution was removed and replaced with egg salts containing the drug of interest. The coverslip was inverted over a circle of Vaseline on a microscope slide, creating a chamber in which the solution on the coverslip could hang. Short bursts of 450-nm nanosecond pulses from a nitrogen-pumped dye laser—part of the optical workstation— were aimed at the viteline membrane causing small perforations to be made through the membrane and eggshell, allowing ingression of the drug. Because the ablation laser was an integral part of the optical workstation, images of the embryo could be collected both before and immediately after the ablation. As a control, dimethyl sulfoxide (DMSO) was used at a 1:100 dilution Latrunculin A (Calbiochem, La Jolla, CA) was used at a concentration of 200 μM nocodazole at a concentration of 25 μg/ml brefeldin A (BFA Molecular Probes Eugene, OR) at a concentration of 150 μg/ml. To increase exposure to the BFA, very early embryos (before eggshell formation) were incubated in 15 μg/ml BFA in blastomere culture medium (Shelton and Bowerman, 1996) and imaged in hanging drops of this solution.


      细胞循环-2 (cell cycle-2 mitosis)

      ok, today we talk about the details about the mitosis.

      We have talked about the general concept of the cell cycle

      And we will look at the interphase first.

      Interphase will have 3 subgroups: the G1,S , and G2

      --During this phase, cells spent its time on growing

      --cells will become mature by making more cytoplasm and organelles

      (explain: we know that 1 parental cell will divide into 2 daughter cells through the mitosis. And these 2 daughter cells were smaller than the parental cell. So just before these 2 daughter cells divide, it need time to grow to its cell size limitation, then, it will divide. Hence, the cell will grow through G1)

      --the cells also carry on its metabolic activity

      --During this time, the DNA is copied and the chromosomes are duplicated

      (We know that the DNA is the genetic information and that each chromosome is composed of a single, tightly coiled DNA molecule.)

      --Cell growth also happened in this phase, and it all the structures needed for the cell division are made

      Then, we talk about the mitosis

      It has 4 stages, prophase, metaphase, anaphase, and telopahse

      We will divide the prophase into early-prophase and late-prophase.

      1. Chromatin in nucleus condenses to form visible chromosomes

      ( and chromatin is the relax form of chromosomes)

      2. Mitotic spindle forms from fibers in cytoskeleton (plant) or centrioles (animal)

      the prophase

      3. two Centrioles move to the both polar of the cell

      the centrioles

      4. Microtubules grow from the centrioles.

      1. Nuclear membrane & nucleolus are broken down

      2. Chromosomes continue condensing and they are clearly visible

      3. Spindle fibers called kinetochores attach to the centromere of each chromatid

      (I think that we should know the relationship between the centromere and kinetochore

      that kinetochore is part of the centromere that used to be attached by the spindle fiber during metaphase)

      4. Spindle finishes forming between the poles of the cell

      During this phase, the s ister chromatids attached to the kinetochore fibers, move to the center of the cell, where is called the metaphase plate

      1. Sister chromatids are pulled apart to opposite poles of the cell by kinetochore fibers and it occured rapidly.

      ( Separating sister chromatids also has a complete set of DNA/Chromosomes)

      Then, the last phase of the mitosis, the telophase.

      Sister chromatids at opposite polesSpindle disassembles

      Chromosomes relaxed and reappear as chromatin

      DNA gets rolled up into a ball again

      Through this image, we can find that(from up to down, from left to right)

      the first one is prophase, the 2nd one is metaphase, the 3rd one is anaphase and the 4th one is the telophase.

      Next , the cytokinesis , and it also means the division of the cytoplasm

      (and part of it has repeated with the mitosis, that cytokinesis occured during anaphase, and through the telophase)

      The parental cell divide into two, identical halves called daughter cellsIn plant cells,

      cell plate forms at the equator to divide cell

      In animal cells, cleavage furrow forms to split cell

      Next time, we will talk about the daughter cells of the parent cell and what will happened if the cell cycle cannot controlled.


      Bio Unit 9 - Lecture notes 9

       Cell grows by producing proteins and organelles, copies its chromosomes and prepares for cell division subdivisions o G1 (Gap 1): most of a cell’s growth o S (Synthesis) phase: DNA copied  Chromosomes attached at centromeres, still fully extended o G2 (Gap 2): cell completes preparations for mitosis  Chromosomes start to condense  Spindle apparatus starts to form

      M Phase (Mitosis and Cytokinesis)

       Subdivided according to state f chromosomes o Chromosomes finally condensed enough to become visible at prophase

      Need 2 cytoskeletal structures for cell division

      Cytokinesis: Animal vs. Plant Cells

      Animal: involves ring of actin filaments just under plasma membrane, in association with motor proteins (myosin)

      Plant: new wall must be constructed between dividing plant cells

      Cytokinesis in Plant Cells

      -Tubulin protein synthesized during G -Actin and myosin filaments crosses one another to cause contraction

      -Microtubules and proteins define and organize the regions where new cell membrane and cell wall form Vesicles mostly from Golgi arrive, carrying polysaccharides and glycoproteins to lay down matrix for new cell wall Later cellulose fibres are laid down to complete wall

      Meiosis I – Meta/Ana/Telophase (Separating homologs) Meiosis II – Separating Chromatids

      Segregation of Homologs in Meiosis I/Chromatids in Meiosis II

      Non-Disjunction of Chromosome 21 in Meiosis I

      How common is aneuploidy in humans?

       Aneuploidy is astonishingly common and extremely important clinically in our species  It accounts for &gt20% of pregnancy losses which most results in ‘miscarriages’  Exceptions: trisomy 21 and 18 which leads to sex chromosome abnormalities  Humans have very high rates in aneuploidy due to mistakes in meiosis and mitosis

      Mistakes in Meiosis -Improper distribution of chromosomes to each daughter cell (“non-disjunction”) -Results in gametes with abnormal # chromosomes (“aneuploidy”) -Extra (third copy: trisomy, one copy: monosomy -Can occur during meiosis I (separation of homologs) or meiosis II (separation of chromatids)

      Meiosis and Sexual Reproduction

       Each cell produced by meiosis receives a different combination of chromosomes o Different complement of genes o Offspring genetically distinct from each other and from their parents  Haploid gametes (n) fuse at fertilization, restoring normal complement of chromosomes (2n)

       Division of genetic material to produce daughter cells with half the hereditary material found in the parent cell  Involved only in the production of gametes (eggs and sperm)

      Sources of Variation in Meiosis

      Advantages of Sexual Reproduction

       Allows natural selection against deleterious alleles of genes o Genetic variation better equips a species to survive environmental changes

      Control of the cell cycle

      Some cells opt out of the cell cycle

       Some cells divide very slowly but can be induced to re-enter cell cycle (liver cells)  Some cells become highly specialized and can no longer divide (terminally differentiated such as neurons or muscle cells)  If cells aren’t cycling then they opt out of the cell cycle and go into G0 or Gnot  It steps out of the cycle but still does its job, instead of duplicating itself

      Control of the cell cycle

       Factor in mammalian cells that induce mitosis is called mitosis promoting factor (MPF)  MPF is a 2 part protein o Cyclin-dependent kinase (Cdk) is a catalytic subunit that transfers phosphate from ATP to certain amino acids on target proteins. It is not active unless bound to cyclin partner o Cyclin- regulatory subunit and levels oscillate throughout the cell cycle  Increase mCdk if you increase cyclin concentration. Requires mCdk to push cell to perform cell cycle

      Alternatives to Meiosis: Asexual reproduction  An organism well adapted to its environment can ‘clone’ itself at an incredibly rapid rate o Bacteria and archaebacteria o Many protists (though can often switch to sexual under stress) o Many plants o Fungi (budding in yeast) o Some insects, fish and reptiles

       Checking in G1 phase if DNA is replicated properly will then be ready to divide. If it is not okay then the DNA will not be replicated and the cell cycle will stop by using cdk inhibitors. But if the cell can’t fix itself then it kills itself

      Three Major Checkpoints in the Cell Cycle

       Tumor suppressors: link cell cycle to DNA damage  Proteins That detect DNA damage and initiate events that halt the cell cycle  Typically transcription factors that drive expression of genes that code for proteins that inhibit Cdks  P53 detects DNA damage at G1/S checkpoint which leads to synthesis of inhibitor F1/S-Cdk and S-Cdk o Loss of p53 (both copies) found in people with cancer

       Suppresses G1/S-Cdk and S-Cdk following DNA damage  Transcriptionally regulated by p

       Suppresses G1/S-Cdk and S-Cdk in G  Helps cells withdraw from cell cycle

       Suppresses G1-Cdk  Frequently inactivated in cancer cells

      E2F: gene regulatory protein that binds to promoters of many genes that encode for proteins for S-phase

      Rb protein: binds to E2F during G1 and blocks transcription of S-phase genes which blocks cell cycle progression

      Dysregulation of Cell Cycle- Accelerators

       If signal pathway pushing cell cycle gets permanently stuck on then cell division is no longer controlled  Can be due to: over-expression of signals promoting cell cycle mutations in signal molecules, their receptors or any molecules in downstream pathway  Oncogene (oncoprotein): mutated versions of normal genes/proteins involved in driving cell division

      How does Cancer start? Cancer initiates as a failure to respect cell cycle checkpoints, particularly G1/S checkpoint

      Control of cell number and cell size

       Decreasing cell number: o Apoptosis-programmed cell death o Getting rid of unwanted cells o Another death process: Necrosis  Increasing cell number ad/or size: o Survival factors: preventing apoptosis o Mitogens: driving the cell cycle o Growth factors: increasing cell size

       Growth is often coupled with cell division  But the two activities can also be separated o Neurons, muscle cells permanently stop dividing then start to grow/specialize (terminally differentiated)  Signals that negatively regulate growth (oppose actions of growth factors)


      Watch the video: HKDSE Biology - Cell Cycle and Division Part 1 (September 2022).


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