During What Phase of Mitosis Do Two Cellular Membranes Begin to Appear

Thousand stage is the most dramatic menstruum of the cell cycle, involving a major reorganization of virtually all cell components. During mitosis (nuclear division), the chromosomes condense, the nuclear envelope of nearly cells breaks down, the cytoskeleton reorganizes to form the mitotic spindle, and the chromosomes move to reverse poles. Chromosome segregation is then usually followed by cell segmentation (cytokinesis). Although many of these events have been discussed in previous chapters with respect to the structure and function of the nucleus and cytoskeleton, they are reviewed here in the context of a coordinated view of M phase and the action of MPF.

Stages of Mitosis

Although many of the details of mitosis vary amongst different organisms, the central processes that ensure the faithful segregation of sis chromatids are conserved in all eukaryotes. These basic events of mitosis include chromosome condensation, formation of the mitotic spindle, and zipper of chromosomes to the spindle microtubules. Sister chromatids and so carve up from each other and move to opposite poles of the spindle, followed by the formation of girl nuclei.

Mitosis is conventionally divided into four stages—prophase, metaphase, anaphase, and telophase—which are illustrated for an animal cell in Figures 14.23 and 14.24. The start of prophase is marked by the appearance of condensed chromosomes, each of which consists of two sister chromatids (the daughter Deoxyribonucleic acid molecules produced in S phase). These newly replicated DNA molecules remain intertwined throughout S and G_ii, becoming untangled during the process of chromatin condensation. The condensed sister chromatids are then held together at the centromere, which (every bit discussed in Affiliate 4) is a DNA sequence to which proteins bind to class the kinetochore—the site of eventual zipper of the spindle microtubules. In addition to chromosome condensation, cytoplasmic changes leading to the development of the mitotic spindle initiate during prophase. The centrosomes (which had duplicated during interphase) separate and motion to opposite sides of the nucleus. In that location they serve as the two poles of the mitotic spindle, which begins to grade during late prophase.

Figure 14.23

Stages of mitosis in an animal cell. During prophase, the chromosomes condense and centrosomes move to reverse sides of the nucleus, initiating formation of the mitotic spindle. Breakdown of the nuclear envelope and then allows spindle microtubules to attach (more...)

Figure 14.24

Fluorescence micrographs of chromatin, keratin, and microtubules during mitosis of newt lung cells. Chromatin is stained blue, keratin is stained crimson, and microtubules are stained green. (Conly L. Rieder/ Biological Photo Service.)

In higher eukaryotes the cease of prophase corresponds to the breakup of the nuclear envelope. Every bit discussed in Affiliate viii, yet, nuclear envelope breakup is not a universal feature of mitosis. In item, yeasts and many other unicellular eukaryotes undergo "closed mitosis," in which the nuclear envelope remains intact (see Figure 8.thirty). In these cells the spindle pole bodies are embedded within the nuclear envelope, and the nucleus divides in two post-obit migration of daughter chromosomes to opposite poles of the spindle.

Following completion of prophase, the jail cell enters prometaphase—a transition period between prophase and metaphase. During prometaphase the microtubules of the mitotic spindle attach to the kinetochores of condensed chromosomes. The kinetochores of sister chromatids are oriented on opposite sides of the chromosome, and so they attach to microtubules emanating from reverse poles of the spindle. The chromosomes shuffle dorsum and forth until they eventually align on the metaphase plate in the eye of the spindle. At this stage, the cell has reached metaphase.

Most cells remain only briefly at metaphase before proceeding to anaphase. The transition from metaphase to anaphase is triggered past breakage of the link between sister chromatids, which then separate and move to contrary poles of the spindle. Mitosis ends with telophase, during which nuclei re-class and the chromosomes decondense. Cytokinesis unremarkably begins during late anaphase and is almost complete by the end of telophase, resulting in the formation of ii interphase daughter cells.

MPF and Progression to Metaphase

Mitosis involves dramatic changes in multiple cellular components, leading to a major reorganization of the entire structure of the prison cell. As discussed before in this chapter, these events are initiated by activation of the MPF poly peptide kinase (Cdc2/cyclin B). It appears that MPF not merely acts equally a master regulator of the M phase transition, phosphorylating and activating other downstream protein kinases, but also acts directly by phosphorylating some of the structural proteins involved in this cellular reorganization (Figure fourteen.25).

Effigy fourteen.25

Targets of MPF. MPF induces multiple nuclear and cytoplasmic changes at the onset of One thousand phase, both by activating other protein kinases and past phosphorylating proteins such as condensins and the nuclear lamins.

The condensation of interphase chromatin to grade the meaty chromosomes of mitotic cells is a key issue in mitosis, disquisitional in enabling the chromosomes to move along the mitotic spindle without condign cleaved or tangled with one another. Every bit discussed in Affiliate 4, the chromatin in interphase nuclei condenses nearly a thousand fold during the formation of metaphase chromosomes. Such highly condensed chromatin cannot be transcribed, so transcription ceases every bit chromatin condensation takes place. Despite the primal importance of this outcome, we practice not fully empathise either the construction of metaphase chromosomes or the molecular mechanism of chromatin condensation. Even so, protein complexes chosen condensins have recently been found to drive chromosome condensation by wrapping DNA around itself, compacting chromosomes into the condensed mitotic structure. The condensins are phosphorylated directly by the Cdc2 protein kinase, which drives chromatin condensation by activating condensins as cells enter mitosis. I molecular amending that by and large accompanies chromosome condensation is phosphorylation of histone H1, and so it is noteworthy that histone H1 is also a substrate for Cdc2. Withal, histone H1 phosphorylation is non required for mitotic chromosome condensation, so the significance of H1 phosphorylation by Cdc2 is unclear. In contrast, chromosome condensation has been shown to crave phosphorylation of histone H3. Perhaps surprisingly, however, histone H3 is not phosphorylated past Cdc2 and the kinase responsible for H3 phosphorylation in mitotic cells remains to be identified.

Breakdown of the nuclear envelope, which is one of the most dramatic events of mitosis, represents the virtually clearly defined target for MPF activeness. Equally discussed in Chapter viii, Cdc2 phosphorylates the lamins, leading directly to depolymerization of the nuclear lamina (come across Figure viii.31). This is followed past fragmentation of the nuclear membrane into minor vesicles, which eventually fuse to form new daughter nuclei at telophase. The endoplasmic reticulum and Golgi appliance similarly fragment into minor vesicles, which can then be distributed to girl cells at cytokinesis. The breakdown of these membranes is besides induced by MPF, and may in part be mediated by Cdc2 phosphorylation of the Golgi matrix protein GM130, which is required for the docking of COPI-coated vesicles to the Golgi membrane. Phosphorylation and inactivation of GM130 by Cdc2 inhibits vesicle docking and fusion, leading to fragmentation of the Golgi appliance. Nevertheless, additional targets of Cdc2 may also be involved, and the mechanisms by which MPF leads to membrane fragmentation remain to be fully elucidated.

The reorganization of the cytoskeleton that culminates in formation of the mitotic spindle results from the dynamic instability of microtubules (see Chapter 11). At the beginning of prophase, the centrosomes motility to opposite sides of the nucleus. The ascent in MPF activity then induces a dramatic alter in the dynamic behavior of microtubules. Kickoff, the charge per unit of microtubule disassembly increases, resulting in depolymerization and shrinkage of the interphase microtubules. This disassembly is thought to result from phosphorylation of microtubule-associated proteins, either by MPF itself or by other MPF-activated protein kinases. In addition, the number of microtubules emanating from the centrosomes increases, so the interphase microtubules are replaced by large numbers of curt microtubules radiating from the centrosomes.

The breakdown of the nuclear envelope and so allows some of the spindle microtubules to attach to chromosomes at their kinetochores (Figure 14.26), initiating the process of chromosome motion that characterizes prometaphase. The proteins assembled at the kinetochore include microtubule motors that straight the motion of chromosomes toward the minus ends of the spindle microtubules, which are anchored in the centrosome. The activity of these proteins, which draw chromosomes toward the centrosome, is opposed by the growth of the spindle microtubules, which pushes the chromosomes away from the spindle poles. Consequently, the chromosomes in prometaphase shuffle back and forth between the centrosomes and the centre of the spindle.

Effigy 14.26

Electron micrograph of microtubules attached to the kinetochore of a chromosome. (Conly L. Rieder/ Biological Photo Service.)

Microtubules from opposite poles of the spindle eventually adhere to the two kinetochores of sister chromatids (which are located on opposite sides of the chromosome), and the balance of forces interim on the chromosomes leads to their alignment on the metaphase plate in the center of the spindle (Effigy xiv.27). As discussed in Chapter eleven, the spindle consists of both kinetochore microtubules, which are attached to the chromosomes, and polar microtubules, which overlap with one some other in the center of the prison cell. In addition, brusk astral microtubules radiate outward from the centrosomes toward the jail cell periphery.

Effigy fourteen.27

The metaphase spindle. (A) The spindle consists of iii kinds of microtubules. Kinetochore microtubules are attached to chromosomes, polar microtubules overlap in the center of the jail cell, and astral microtubules radiate from the centrosome to the prison cell (more than...)

Proteolysis and the Inactivation of MPF: Anaphase and Telophase

As discussed before in this affiliate, an important cell cycle checkpoint monitors the alignment of chromosomes on the metaphase spindle. In one case this has been accomplished, the cell proceeds to initiate anaphase and complete mitosis. The progression from metaphase to anaphase results from ubiquitin-mediated proteolysis of key regulatory proteins, triggered by activation of a ubiquitin ligase (see Figure seven.39) called the anaphase-promoting circuitous. Activation of the anaphase-promoting complex is induced by MPF at the beginning of mitosis, so MPF ultimately triggers its own destruction. The anaphase-promoting complex remains inhibited, however, until the cell passes the metaphase checkpoint, after which activation of the ubiquitin degradation system brings nearly the transition from metaphase to anaphase and progression through the rest of mitosis.

Activation of the anaphase-promoting complex leads to the degradation of at least two key regulatory proteins (Figure 14.28). The onset of anaphase results from proteolytic degradation of a protein called Scc1, a component of a complex of proteins called cohesins that maintain the connection between sister chromatids while they are aligned on the metaphase plate. Degradation of Scc1 is non catalyzed direct by the anaphase-promoting complex, which instead degrades a regulatory protein called Pds1. Degradation of Pds1 in plough activates another protein, called Esp1, which leads to proteolysis of the cohesin Scc1. Cleavage of Scc1 breaks the linkage between sister chromatids, allowing them to segregate by moving to opposite poles of the spindle (Figure xiv.29). The separation of chromosomes during anaphase and so proceeds as a result of the action of several types of motor proteins associated with the spindle microtubules (see Figures 11.48 and 11.49).

Figure 14.28

Targets of the cyclin B proteolysis arrangement. The anaphase-promoting circuitous is a ubiquitin ligase that is activated following passage through the metaphase checkpoint. Its activation brings most the transition from metaphase to anaphase by leading to (more...)

Figure xiv.29

A whitefish jail cell at anaphase. (Michael Abbey/Photo Researchers, Inc.)

The other cardinal regulatory protein targeted for ubiquitination and degradation past the anaphase-promoting complex is cyclin B. Degradation of cyclin B leads to inactivation of MPF, which is required for the prison cell to get out mitosis and return to interphase. Many of the cellular changes involved in these transitions are only the reversal of the events induced past MPF during entry into mitosis. For instance, reassembly of the nuclear envelope, chromatin decondensation, and the render of microtubules to an interphase land probably result directly from loss of MPF activity and dephosphorylation of proteins that had been phosphorylated by MPF at the kickoff of mitosis. As discussed next, inactivation of MPF also triggers cytokinesis.

Cytokinesis

The completion of mitosis is usually accompanied by cytokinesis, giving ascent to two daughter cells. Cytokinesis usually initiates in late anaphase and is triggered by the inactivation of MPF, thereby coordinating nuclear and cytoplasmic sectionalization of the cell. Every bit discussed in Chapter 11, cytokinesis of animal cells is mediated by a contractile band of actin and myosin II filaments that forms beneath the plasma membrane (Effigy 14.30). The location of this ring is adamant by the position of the mitotic spindle, and so the cell is somewhen broken in a airplane that passes through the metaphase plate perpendicular to the spindle. Cleavage proceeds as contraction of the actin-myosin filaments pulls the plasma membrane in, eventually pinching the jail cell in half.

Figure 14.thirty

Cytokinesis of animal cells. (A) Cytokinesis results from contraction of a ring of actin and myosin filaments, which pinches the jail cell in 2. (B) Scanning electron micrograph of a frog egg undergoing cytokinesis. (B, David Thousand. Phillips/Visuals Unlimited). (more than...)

The mechanism of cytokinesis is different for college establish cells, which are surrounded by rigid cell walls. Rather than being pinched in half by a contractile ring, these cells split up by forming new cell walls and plasma membranes inside the cell (Figure 14.31). In early telophase, vesicles carrying cell wall precursors from the Golgi appliance associate with spindle microtubules and accumulate at the onetime site of the metaphase plate. These vesicles then fuse to form a big, membrane-enclosed, disclike structure, and their polysaccharide contents assemble to form the matrix of a new cell wall (called a cell plate). The cell plate expands outward, perpendicular to the spindle, until information technology reaches the plasma membrane. The membrane surrounding the prison cell plate then fuses with the parental plasma membrane, dividing the prison cell in two.

Figure fourteen.31

Cytokinesis in college plants. Golgi vesicles conveying cell wall precursors acquaintance with polar microtubules at the former site of the metaphase plate. Fusion of these vesicles yields a membrane-enclosed, disclike structure (the early cell plate) that (more than...)

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Source: https://www.ncbi.nlm.nih.gov/books/NBK9958/