mod 11 chap 11 +14.1 Flashcards
The Cell Cycle
Cell division is the process by which a single cell produces two daughter cells. In order for a cell to divide successfully, it must be large enough to divide in two and contribute sufficient nuclear and cytoplasmic components to each daughter cell. Before the cell divides, therefore, key cellular components are duplicated, including DNA. DNA replication followed by cell division is achieved in a series of steps that constitutes the cell cycle, which describes the life cycle of a cell.
life cycle of the cell begins and ends with cell division
Prokaryotic cells divide by binary fission
Prokaryotic cells produce daughter cells by binary fission. In this form of cell division, a cell replicates its DNA, increases in size, and divides into two daughter cells. Each daughter cell receives one copy of the replicated parental DNA. Binary fission has been studied most extensively in bacteria. The process of binary fission is similar in archaea as well as in chloroplasts and mitochondria, organelles within plant, fungal, and animal cells that evolved from free-living prokaryotic cells
Let’s consider the process of binary fission in the intestinal bacterium Escherichia coli (Fig. 11.1). The circular genome of E. coli is attached by proteins to the inside of the cell membrane (Fig. 11.1, step 1). Binary fission begins with DNA replication. Replication is initiated at a specific location on the circular DNA molecule, called the origin of replication, and proceeds in opposite directions around the circle. The result is two DNA molecules, each attached to the cell membrane at a different site. The two attachment sites are initially close together (Fig. 11.1, step 2). The cell then elongates, and, as it does so, the two DNA attachment sites move apart (Fig. 11.1, steps 3 and 4). When the cell is about twice its original size and the DNA molecules are well separated, a constriction forms at the midpoint of the cell (Fig. 11.1, step 5). Eventually, new membrane and cell wall are synthesized at the site of the constriction, dividing the single cell into two (Fig. 11.1, step 6). The result is two daughter cells, each having the same genetic material as the parent cell.
Like most cellular processes, binary fission requires the coordination of many components, including several genes whose products play a key role. One of these genes, called FtsZ, has been especially well studied. FtsZ encodes a protein that forms a ring at the site of constriction where the new cell wall forms between the two daughter cells. FtsZ is present in the genomes of diverse bacteria and archaea, suggesting that it plays a fundamental role in binary fission. Interestingly, it appears to be evolutionarily related to the protein tubulin. Recall from Chapter 10 that tubulin makes up microtubules found in eukaryotic cells that are important in intracellular transport, cell movement, and cell division.
Eukaryotic cells divdie by mitotic cell division
The basic steps of binary fission that we just discussed — replication of DNA, segregation of replicated DNA to daughter cells, and division of one cell into two — occur in all forms of cell division. However, cell division in eukaryotes is more complicated than cell division in prokaryotes. When eukaryotic cells divide, they first divide the nucleus by mitosis and then divide the cytoplasm into two daughter cells by cytokinesis. Together, these two processes are called mitotic cell division.
The genetic material in cells is packaged into chromosomes, which consist of a single DNA molecule and associated proteins, but the organization of chromosomes is different in prokaryotic and eukaryotic cells. The genome of a prokaryotic cell is organized as a single, relatively small, circular chromosome. By contrast, the genome of a eukaryotic cell is typically much larger and is organized into one or more linear chromosomes. Each of these chromosomes must be replicated and separated into daughter cells. The DNA of prokaryotes is attached to the inside of the cell membrane, allowing replicated DNA to be separated into daughter cells by cell growth. By contrast, the DNA of eukaryotes is located in the nucleus. As a result, eukaryotic cell division requires first the breakdown and then the re-formation of the nuclear envelope, as well as mechanisms other than cell growth to separate replicated DNA. As we saw in Chapter 10 and discuss in more detail in section 11.4, chromosomes of dividing eukaryotic cells attach to the mitotic spindle, which separates them into daughter cells.
Interestingly, some unicellular eukaryotes exhibit forms of cell division that have characteristics of both binary fission and mitotic cell division. For example, dinoflagellates, like all eukaryotes, have a nucleus and linear chromosomes. However, unlike in most eukaryotes, the nuclear envelope does not break down but stays intact during cell division. Furthermore, the replicated DNA is attached to the nuclear envelope. The nucleus then grows and divides in a manner reminiscent of binary fission. These and other observations of intermediate forms of cell division strongly suggest that mitosis evolved from binary fission.
The cell cycle proceeds in phases
Cell division is one of a number of steps that make up the cell cycle (Fig. 11.2). The cell cycle consists of two phases: M phase and interphase. During M phase, the parent cell divides into two daughter cells. M phase consists of two different events: (1) mitosis, the separation of the chromosomes into two nuclei, and (2) cytokinesis, the division of the cell itself into two separate cells. Typically, these two processes go hand in hand, with cytokinesis beginning even before mitosis is complete. In most mammalian cells, M phase lasts about an hour.
Interphase is the time between two successive M phases (Fig. 11.2). During interphase, the cell makes many preparations for division. These preparations include DNA replication and cell growth. The DNA in the nucleus first replicates so that each daughter cell receives a copy of the genetic material. The cell then increases in size so that each daughter cell receives sufficient amounts of cytoplasmic and membrane components to allow it to survive on its own. Organelles such as mitochondria are also organized by the cytoskeleton to ensure they are partitioned about equally to each daughter cell.
Interphase is idivded into three phases
dna rep occurs in S phase
its called s phase bc dna rep involved the synthesis of DNA
mostly S phase doesnt immedtly precede or follow mitosis buts its sperated from it by the gap phases: G1 and G2
many essential processes occur in these phases
during G1, regulatory proteins like kinases are made
these proteins actiavte enzymes that synetshize DNA
in G2 both the side and protein content of the cell inc
so G1 is time of prep for S phase and G2 is time of prpep for mitosis amd cytokinses
How long a cell takes to pass through the cell cycle depends on the type of cell and the organism’s stage of development. Most actively dividing cells in your body take about 24 hours to complete the cell cycle. Cells in your skin and intestine that require frequent replenishing usually take about 12 hours.
not all the cells in the body actievly divide
many pause bewteen M and S phase for perods ranging from day sto more thna a year
this period is G0 phase
its seperated by G1 by the absecne of prep for DNA syntheiss
Liver cells remain in G0 for a year
other cells like nerves enter G0 permantly bc they are non divding
althouh cells in G0 have exited the cell cycle they are active in otehr ways like eprofming their specilized functions
like liver cells stillc arry out metabolsima dn detoxifatcion
DNA replication
Before a cell divides, DNA must be replicated so that each of the daughter cells receives genetic information from a parent cell. Faithful replication enables DNA to pass genetic information from cell to cell and from parent to offspring. As a result, DNA replication is the molecular basis for inheritance.
double-stranded DNA consists of a pair of deoxyribonucleotide polymers wound around each other in antiparallel helical coils in such a way that a purine base (A or G) in one strand is paired with a pyrimidine base (T or C, respectively) in the other strand. To say that the strands are antiparallel means that they run in opposite directions: one strand runs in the5’ to 3’ direction and the other runs in the 3’ to 5’ direction. These key elements of DNA structure are the only essential pieces of information needed to understand the mechanism of DNA replication.
DNA replicates semiconsevrtly
When Watson and Crick published their paper describing the structure of DNA using crucial structural data obtained by Rosalind Franklin, they also coyly laid claim to another discovery: “It has not escaped our notice that the specific pairing we have postulated [A with T, and G with C] immediately suggests a copying mechanism for the genetic material.” The copying mechanism they had in mind is exquisitely simple. The two strands of the parental DNA double helix unwind and separate into single strands at a site called the replication fork (Fig. 11.3). Each individual parental strand serves as a model, or template strand, for the synthesis of a daughter strand. As each daughter strand is synthesized, the order of the bases in the template strand determines the order of the complementary bases added to the daughter strand.
A key aspect of the model shown in Fig. 11.3 is semiconservative replication. That is, after replication, each new DNA molecule consists of one strand that was originally part of the parental molecule and one newly synthesized strand. An alternative model is conservative replication, which proposes that the original DNA molecule remains intact and the daughter DNA molecule is completely new. Which model is correct? If there were a way to distinguish newly synthesized daughter DNA strands (“new strands”) from previously synthesized parental strands (“old strands”), the products of replication could be observed and the mode of replication determined.
American molecular biologists Matthew S. Meselson and Franklin W. Stahl carried out an experiment to determine how DNA replicates. This experiment, described in Fig. 11.4, has been called “the most beautiful experiment in biology” because it so elegantly demonstrates the process of generating hypotheses, making predictions, and performing an experiment to test the hypotheses (Chapter 1). Meselson and Stahl found that DNA replicates semiconservatively.
Important as it was in demonstrating semiconservative replication in bacteria, the Meselson–Stahl experiment left open the possibility that DNA replication in eukaryotes might be different. It was only a few years after the Meselson–Stahl experiment that methods for labeling DNA with fluorescent nucleotides were developed. These methods allowed researchers to visualize entire strands of eukaryotic DNA and follow each strand through replication.
Fig. 11.5 shows a human chromosome with unlabeled DNA that subsequently underwent two rounds of replication in medium containing a fluorescent nucleotide. The chromosome was photographed at metaphase of the second round of mitosis, after chromosome duplication but before the separation of the chromatids into the daughter cells. Notice that one chromatid contains hybrid DNA with one labeled strand and one unlabeled strand, which fluoresces faintly (light); the other chromatid contains two strands of labeled DNA, which fluoresces strongly (dark). This result is conceptually the same as what was seen by Meselson and Stahl after two rounds of replication and exactly as predicted by the semiconservative replication model. The result also demonstrates that each eukaryotic chromosome contains a single DNA molecule that runs continuously all along its length.
DNA replictann ivnolves many enzymes
As we have seen, DNA replication begins at a replication fork, where the parental strands separate. Many enzymes are involved in DNA replication, some of which are shown in Fig. 11.6. An enzyme called helicase separates the strands of the parental double helix by breaking hydrogen bonds holding the base pairs together. Then single-strand binding protein binds to these single-stranded regions to prevent the template strands from coming back together. Another enzyme called topoisomerase works upstream from the replication fork to relieve the stress that results from unwinding the double helix at the replication fork. Topoisomerases are a family of enzymes that wind or unwind DNA to help relieve stress that occurs during both replication and transcription. There are two types of topoisomerase depending on the number of DNA strands cut in the first step of topoisomerase action: type I topoisomerases cut one strand of DNA, whereas type II cut both strands of DNA. During DNA replication, topoisomerase II works upstream from the replication fork and relieves the stress on the double helix by unwinding the cut strands in the opposite direction from how they are unwound at the replication fork.
An enzyme called DNA polymerase is a critical component of a large protein complex that carries out DNA replication. DNA polymerases exist in all organisms and are highly conserved, meaning that they vary little from one species to another because they carry out an essential function. A cell typically contains several different DNA polymerase enzymes, each specialized for a particular situation. However, all DNA polymerases share the same basic function in that they synthesize a new DNA strand from an existing template.
DNA polymerase has two properties that are especially important for understanding the details of DNA replication. The first is that it can only attach a nucleotide to another nucleotide. In other words, it can only elongate the end of an existing piece of DNA or RNA and cannot lay down the first nucleotide of a newly synthesized strand on its own. As a result, each new DNA strand must begin with a short stretch of RNA that serves as a primer, or starter, for DNA synthesis (Fig. 11.6). The primer is made by an enzyme called RNA primase, which synthesizes a short piece of RNA complementary to the DNA parental strand. Once the RNA primer has been synthesized, DNA polymerase takes over, adding successive DNA nucleotides to the end of the growing strand.
a second proeprty of DNA polymerse is that it can onlu add nucleotides to the 3’ end of another nucleotide
at the 5’ end is a phosphaye and at the 3’ end its hydroxyl
DNA plymerase can only add a nucelotide to 3’ end
DNA synethssi cocrus whne the 3’ hydroxyl group attacks the phosphate group of an icnoming nucelotide triphosphate
as a result, DNA syntehsis or polymerization occurs only in the 5’ to 3’ direction
as the incimung nucelotide triphaspahet is added, one of the ncelotdies high enegry pshoate bonds is broken providng energy for the rxn
the outer two phsopahes called pyrophosphates are released inthe process
in replication DNA one duaghetr strand is syntehsize continously and the other in pieces
Because the two DNA strands in a double helix are antiparallel and a new DNA strand can be elongated only at the 3’ end, the two daughter strands are synthesized in quite different ways (Fig. 11.8). As the replication fork moves along, it creates a region of single-stranded DNA. An RNA primer is first laid down, as shown in the figure. Then DNA polymerase takes over. The daughter strand shown at the bottom of the replicating DNA molecule in Fig. 11.8 has its 3’ end pointed toward the replication fork so that as the parental double helix unwinds, nucleotides can be added onto the 3’end, and this daughter strand can be synthesized as one long, continuous polymer. This daughter strand is called the leading strand.
The situation is different for the daughter strand shown at the top of the replicating DNA molecule in Fig. 11.8. Its 5’ end is near the replication fork, but the strand cannot grow in that direction. To enable synthesis of the top strand, the replication fork moving to the left creates a single-stranded region of parental DNA ranging in length from a few hundred to a few thousand nucleotides. Synthesis of the daughter strand is initiated on this single-stranded stretch of parental DNA with its 5’end near the replication fork. Elongation of the new strand occurs at its 3’ end as usual, which means that the daughter strand grows in a direction away from the replication fork, not toward it. As the parental double helix unwinds, a new RNA primer is laid down at intervals, which is extended by DNA polymerase until it reaches the piece in front of it. The result is that this daughter strand is synthesized in short, discontinuous pieces. This daughter strand is called the lagging strand. The short pieces in the lagging strand are sometimes called Okazaki fragments after their discoverer, Japanese molecular biologist Reiji Okazaki.
The presence of leading and lagging strands during DNA replication is a consequence of the antiparallel nature of the two strands in a DNA double helix and the fact that DNA polymerase can synthesize DNA in only one direction
Because the DNA polymerase complex extends an RNA primer, all new DNA strands have a short stretch of RNA at their 5’ end. For the lagging strand, there are many such primers, one for each of the discontinuous fragments of newly synthesized DNA. As each of these fragments is elongated by DNA polymerase, it grows toward the primer of the fragment in front of it (Fig. 11.9). When the growing fragment comes into contact with the primer of the fragment synthesized earlier, a different DNA polymerase complex takes over, removing the earlier RNA primer and extending the growing fragment with DNA nucleotides to fill the space left by its removal. When the replacement is completed, the adjacent fragments are joined, or ligated, by an enzyme called DNA ligase.
The DNA polymerase complexes for each strand stay in contact with each other so that synthesis of the leading and lagging strands is coordinated to occur at the same time and rate (Fig. 11.10). In this arrangement, the lagging strand’s polymerase releases and retrieves the lagging strand for the synthesis of each new RNA primer. The positioning of the polymerases is such that both the leading strand and the lagging strand pass through in the same direction, which requires that the lagging strand be looped around as shown in Fig. 11.10. In this configuration, the 3’ end of the lagging strand and the 3’ end of the leading strand are elongated together, which ensures that neither strand outpaces the other in its rate of synthesis. The depiction of DNA replication shown in Fig. 11.10 is sometimes called the trombone model.
DNA polymerase is self correcting bc of its proofreading function
Most DNA polymerases can correct their own errors in a process called proofreading, which is a separate enzymatic activity from strand elongation (synthesis) (Fig. 11.11). When each new nucleotide comes into line in preparation for attachment to the growing DNA strand, the nucleotide is temporarily held in place by hydrogen bonds that form between the base in the new nucleotide and the base across the way in the template strand. The strand being synthesized and the template strand therefore have complementary bases — A paired with T, or G paired with C.
However, on rare occasions, an incorrect nucleotide is attached to the new DNA strand. When this happens, DNA polymerase can correct the error because it detects mispairing between the template and the most recently added nucleotide. Mispairing between a base in the parental strand and a newly added base in the daughter strand activates a DNA-cleavage function of DNA polymerase that removes the incorrect nucleotide and inserts the correct one in its place.
Mutations resulting from errors in nucleotide incorporation still occur, but proofreading reduces their number. In the bacterium E. coli, for example, about 99% of the incorrect nucleotides that are incorporated during replication are removed and repaired by the proofreading function of DNA polymerase. Those that slip past proofreading and other repair systems lead to mutations, which are then faithfully copied and passed on to daughter cells. Some of these mutations may be harmful, but others are neutral and a rare few may be beneficial. These mutations are the ultimate source of genetic variation that we see among individuals of the same species and among species
Replication of chromosomes
The basic steps involved in semiconservative DNA replication are universal, suggesting that they evolved in the common ancestor of all living organisms. In addition, they are the same whether they occur in a test tube or in a cell, or whether the segment of DNA being replicated is short or long. However, the replication of an entire linear chromosome poses particular challenges. Here, we consider two such challenges encountered by cells in replicating their chromosomes: how replication starts and how it ends.
Replication of DNA in chromosomes starts at many places almost simultaneously
DNA replication is relatively slow. In eukaryotes, it occurs at a rate of about 50 nucleotides per second. At this rate, replication from end to end of the DNA molecule in the largest human chromosome would take almost two months. In fact, it takes only a few hours. This fast pace is possible because in a long DNA molecule, replication begins almost simultaneously at many places. Each point at which DNA synthesis is initiated is called an origin of replication. The opening of the double helix at each origin of replication forms a replication bubble. with a replication fork on each side, each with a leading strand and a lagging strand with topoisomerase II, helicase, and single-strand binding protein playing their respective roles (Fig. 11.12). DNA synthesis takes place at each replication fork, and as the replication forks move in opposite directions, the replication bubble increases in size. When two replication bubbles meet, they fuse to form one larger replication bubble.
Note in Fig. 11.12 that within a single replication bubble, the same daughter strand is the leading strand at one replication fork and the lagging strand at the other replication fork. This situation results from the fact that the replication forks in each replication bubble move away from each other. When two replication bubbles fuse and the leading strand from one meets the lagging strand from the other, the ends of the strands that meet are joined by DNA ligase, just as happens when the discontinuous fragments within the lagging strand meet
Some DNA molecules, including most of the DNA molecules in bacterial cells and the DNA in mitochondria and chloroplasts (Chapter 3), are small circles, not long, linear molecules. Such circular DNA molecules typically have only one origin of replication (Fig. 11.13). Replication takes place at both replication forks, and the replication forks proceed in opposite directions around the circle until they meet and fuse on the opposite side, completing one round of replication.
Telomerase restores tips of linear chromosomes shortened during DNA replication
A circular DNA molecule can be replicated completely because it has no ends, and the replication forks can move completely around the circle (Fig. 11.13). Linear DNA molecules have ends, however, and at each round of DNA replication, the ends become slightly shorter.
Recall that each fragment of newly synthesized DNA starts with an RNA primer. On the leading strand, the only primer required is at the origin of replication when synthesis begins. The leading strand is elongated in the same direction as the moving replication fork and is able to replicate the template strand all the way to the end. On the lagging strand, however, which grows away from the replication fork, many primers are required, and the final RNA primer is synthesized about 100 nucleotides from the end of the template. Because this primer initiates synthesis of the final Okazaki fragment of the lagging strand, no other Okazaki fragment is available to synthesize the missing 100 base pairs and remove the primer. Therefore, when DNA replication is complete, the new daughter DNA strand will be missing about 100 base pairs from the tip (plus a few more owing to the length of the primer). When this new daughter strand is replicated, the newly synthesized strand must terminate at the shortened end of the template strand, so the new molecule is shortened by about 100 base pairs from the original parental molecule. The strand shortening in each round of DNA replication is a problem because without some mechanism to restore the tips, the DNA in the chromosome would eventually be nibbled away to nothing.
Eukaryotic organisms have evolved mechanisms that solve the problem of shortened ends (Fig. 11.15). Each end of a eukaryotic chromosome is capped by a repeating sequence called the telomere. The repeating sequence that constitutes the telomere differs from one group of organisms to the next, but in the chromosomes of humans and other vertebrates, it consists of the sequence repeated over and over again in about 1500–3000 copies. For simplicity, just four copies of this telomere sequence are shown in Fig. 11.15. The telomere is slightly shortened in each round of DNA replication, as shown in Fig. 11.14, but the shortened end is quickly restored by an enzyme known as telomerase, which contains an RNA molecule complementary to the telomere sequence.
As shown in Fig. 11.15, the telomerase replaces the lost telomere repeats by using its RNA molecule as a guide to add successive DNA nucleotides to the end of the template strand. Once the end of the template strand has been elongated, an RNA primer and the complementary DNA strand are synthesized. In this way, the original telomere is completely restored. Because no genes are present in the telomere, the slight shortening and subsequent restoration that take place have no harmful consequences.
Telomerase activity differs from one cell type to the next. It is fully active in germ cells, which produce sperm or eggs, and also in stem cells, undifferentiated cells that can undergo an unlimited number of mitotic divisions and can differentiate into any of a large number of specialized cell types. Stem cells are found in embryos, where they differentiate into all the various cell types of the body (Chapter 18). Stem cells are also found in some tissues of the body after embryonic development, where they replenish cells that have a high rate of turnover, such as blood and intestinal cells, and play a role in tissue repair.
In contrast to the high activity of telomerase in germ cells and stem cells, telomerase is almost inactive in most cells in the adult body. In these cells, the telomeres are nevertheless shortened by about 100 base pairs in each mitotic division. Telomere shortening limits the number of mitotic divisions that the cells can undergo because human cells stop dividing when their chromosomes have telomeres with fewer than about 100 copies of the telomere repeat. Adult somatic cells can therefore undergo only about 50 mitotic divisions until the telomeres are so short that the cells stop dividing.
Many biologists believe that the limit on the number of cell divisions explains, in part, why our tissues become less youthful and wounds heal more slowly with age. The telomere hypothesis of aging is still controversial, but increasing evidence suggests that it is one of several factors that lead to aging. The flip side of the coin is observed in cancer cells, in which telomerase is reactivated and helps support uncontrolled cell growth and division.
Mitotic Division
Following DNA replication, the cell then divides in two. Mitotic cell division (mitosis followed by cytokinesis) is the basis for asexual reproduction in unicellular eukaryotes and the means by which cells, tissues, and organs develop and are maintained in multicellular eukaryotes. During mitosis and cytokinesis, the parental cell’s DNA is passed on to two daughter cells. This process is continuous, but it is divided into discrete steps. These steps are marked by dramatic changes in the cytoskeleton and in the packaging and movement of the chromosomes.
In eukaryotic cells, chromosomes come in pairs called homologous chromosomes
One of the key challenges faced by a dividing eukaryotic cell is ensuring that the daughter cells receive an equal and complete set of chromosomes. The length of DNA contained in the nucleus of an average eukaryotic cell is on the order of 1 to 2 meters, well beyond the diameter of a cell. The DNA therefore is condensed to fit into the nucleus, and then the DNA is further condensed during cell division so that it does not become tangled as it segregates, or separates, into daughter cells.
Every species is characterized by a specific number of chromosomes, and each chromosome contains a single molecule of DNA carrying a specific set of genes. When chromosomes condense and become visible during mitosis, they adopt characteristic shapes and sizes that allow each chromosome to be identified by its appearance under a light microscope. The portrait formed by the number and shapes of chromosomes representative of a species is called its karyotype.
Most of the cells in the human body, with the exception of the gametes, contain 46 chromosomes (Fig. 11.16). By way of comparison, cells of horses have 64 chromosomes, and cells of corn have 20. In a human karyotype, the 46 chromosomes can be arranged into 23 pairs, 22 pairs of chromosomes numbered 1 to 22 from the longest to the shortest chromosome and 1 pair of sex chromosomes. Pairs of chromosomes of the same type carrying the same set of genes are homologous chromosomes. One chromosome in each pair was received from the mother and the other from the father. The sex chromosomes are the X and Y chromosomes. Individuals with two X chromosomes are genetically female, and those with an X and a Y chromosome are genetically male.
The number of complete sets of chromosomes in a cell is known as its ploidy. A cell with one complete set of chromosomes is haploid, represented as n. A cell with two complete sets of chromosomes is diploid, represented as 2n. Some organisms, such as plants, have four (4n) or sometimes more complete sets of chromosomes. Such cells are polyploid.
In order for cell division to proceed, every chromosome in the parent cell must be duplicated so that each daughter cell receives a full set of chromosomes. This duplication occurs during S phase, as we discussed above. Even though the DNA in each chromosome duplicates, the two identical copies, called sister chromatids, do not separate. They stay side by side, physically held together at a constriction called the centromere. At the beginning of mitosis, the nucleus of a human cell still contains 46 chromosomes, but each chromosome is a pair of identical sister chromatids linked together at the centromere (Fig. 11.17). Thus, counting chromosomes is simply a matter of counting centromeres.
During mitosis, the sister chromatids separate from each other and go to opposite ends of the cell so that each daughter cell receives the same number of chromosomes as is present in the parent cell, as we describe now.
Prophase: Chromosomes condense and become visible
Mitosis takes place in five stages, each of which is easily identified by events that can be observed under a microscope (Fig. 11.18). When you look in a microscope at a cell in interphase, you cannot distinguish specific chromosomes because they are long and thin. As the cell moves from G2 phase to the start of mitosis, the chromosomes condense and become visible in the nucleus. This process is called chromosome condensation. During this process, chromosomes undergo a dramatic change in packaging and organization. They change from long, thin, threadlike structures to short, dense forms that are identifiable under a microscope during M phase. The first stage of mitosis is known as prophase and is characterized by the appearance of visible chromosomes
Outside the nucleus, in the cytosol, the cell undergoes dramatic reorganization of the cytoskeleton (Chapter 10). Microtubules assemble into the mitotic spindle, a structure that pulls the chromosomes to opposite ends of the dividing cell. These spindles radiate from the centrosome, a compact structure that is the microtubule organizing center for animal cells. Plant cells also have a mitotic spindle made up of microtubules, but they lack centrosomes.
During S phase in animal cells, the centrosome duplicates and each one begins to migrate around the nucleus. The two centrosomes ultimately halt at opposite poles in the cell at the start of prophase. The final locations of the centrosomes define the opposite ends of the cell that will eventually be separated into two daughter cells. As the centrosomes make their way to the poles of the cell, tubulin dimers assemble around them, forming microtubules that radiate from each centrosome. These radiating filaments form the mitotic spindle and later serve as the guide wires for chromosome movement.
