what aer the events of meiosis that lead to genetic variation?

Answer 1

Random fertilization, independent assortment and "crossing over". Don't ask me to elaborate as my grey cells are winding down for the night and Mitosis / Meiosis coursework is a little on the heavy side....

Answer 2

1. Chiasmata formation- whereby the arms of paired homologous chromosomes cross over and genetic information is swapped.
2. Random homologous pairs- the way they line up at the spindle fibres before being separated in the first division.
3. Meiosis is the production of the gametes and so is not the fertilised egg. So anyone who has put random fertilisation is wrong. It is not a part of meiosis.

Answer 3

To elaborate on the reasons listed by the previous answerer.
Random fertilization is the random release of an egg being fertilised by a random sperm (each genetically different to each other), independent assortment is the lining up of different chromosomes ending up in each gamete (sex cell). as in we have 23 pairs of chromosomes which randomly sort themselves into different gametes.

Finally "crossing over" is from when the pairs of chromosomes line up next to each other before cell division, they can become kind of entwined and the genetic information can swap between pairs of chromosomes.

Regards

Answer 4

Crossing over of chromosomes occurs (during prophase). This is where parts of two different chromatids (duplicated chromosomes) are swapped.

Answer 5

The Events of M Phase

M phase is the most dramatic period of the cell cycle, involving a major reorganization of virtually all cell components. During mitosis (nuclear division), the chromosomes condense, the nuclear envelope of most cells breaks down, the cytoskeleton reorganizes to form the mitotic spindle, and the chromosomes move to opposite poles. Chromosome segregation is then usually followed by cell division (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 among different organisms, the fundamental processes that ensure the faithful segregation of sister chromatids are conserved in all eukaryotes. These basic events of mitosis include chromosome condensation, formation of the mitotic spindle, and attachment of chromosomes to the spindle microtubules. Sister chromatids then separate from each other and move to opposite poles of the spindle, followed by the formation of daughter 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 beginning of prophase is marked by the appearance of condensed chromosomes, each of which consists of two sister chromatids (the daughter DNA molecules produced in S phase). These newly replicated DNA molecules remain intertwined throughout S and G2, becoming untangled during the process of chromatin condensation. The condensed sister chromatids are then held together at the centromere, which (as discussed in Chapter 4) is a DNA sequence to which proteins bind to form the kinetochore—the site of eventual attachment 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 move to opposite sides of the nucleus. There they serve as the two poles of the mitotic spindle, which begins to form during late prophase.

In higher eukaryotes the end of prophase corresponds to the breakdown of the nuclear envelope. As discussed in Chapter 8, however, nuclear envelope breakdown is not a universal feature of mitosis. In particular, yeasts and many other unicellular eukaryotes undergo “closed mitosis,” in which the nuclear envelope remains intact (see Figure 8.30). In these cells the spindle pole bodies are embedded within the nuclear envelope, and the nucleus divides in two following migration of daughter chromosomes to opposite poles of the spindle.

Following completion of prophase, the 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, so they attach to microtubules emanating from opposite poles of the spindle. The chromosomes shuffle back and forth until they eventually align on the metaphase plate in the center 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 by breakage of the link between sister chromatids, which then separate and move to opposite poles of the spindle. Mitosis ends with telophase, during which nuclei re-form and the chromosomes decondense. Cytokinesis usually begins during late anaphase and is almost complete by the end of telophase, resulting in the formation of two interphase daughter cells.top link
MPF and Progression to Metaphase

Mitosis involves dramatic changes in multiple cellular components, leading to a major reorganization of the entire structure of the cell. As discussed earlier in this chapter, these events are initiated by activation of the MPF protein kinase (Cdc2/cyclin B). It appears that MPF not only acts as 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 14.25).

The condensation of interphase chromatin to form the compact chromosomes of mitotic cells is a key event in mitosis, critical in enabling the chromosomes to move along the mitotic spindle without becoming broken or tangled with one another. As discussed in Chapter 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 as chromatin condensation takes place. Despite the fundamental importance of this event, we do not fully understand either the structure of metaphase chromosomes or the molecular mechanism of chromatin condensation. However, protein complexes called 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. One molecular alteration that generally accompanies chromosome condensation is phosphorylation of histone H1, so it is noteworthy that histone H1 is also a substrate for Cdc2. However, histone H1 phosphorylation is not required for mitotic chromosome condensation, so the significance of H1 phosphorylation by Cdc2 is unclear. In contrast, chromosome condensation has been shown to require phosphorylation of histone H3. Perhaps surprisingly, however, histone H3 is not phosphorylated by 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 most clearly defined target for MPF action. As discussed in Chapter 8, Cdc2 phosphorylates the lamins, leading directly to depolymerization of the nuclear lamina (see Figure 8.31). This is followed by fragmentation of the nuclear membrane into small vesicles, which eventually fuse to form new daughter nuclei at telophase. The endoplasmic reticulum and Golgi apparatus similarly fragment into small vesicles, which can then be distributed to daughter cells at cytokinesis. The breakdown of these membranes is also 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 apparatus. However, 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 move to opposite sides of the nucleus. The rise in MPF activity then induces a dramatic change in the dynamic behavior of microtubules. First, the rate 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 short microtubules radiating from the centrosomes.

The breakdown of the nuclear envelope then allows some of the spindle microtubules to attach to chromosomes at their kinetochores (Figure 14.26), initiating the process of chromosome movement that characterizes prometaphase. The proteins assembled at the kinetochore include microtubule motors that direct the movement of chromosomes toward the minus ends of the spindle microtubules, which are anchored in the centrosome. The action 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 center of the spindle.

Microtubules from opposite poles of the spindle eventually attach to the two kinetochores of sister chromatids (which are located on opposite sides of the chromosome), and the balance of forces acting on the chromosomes leads to their alignment on the metaphase plate in the center of the spindle (Figure 14.27). As discussed in Chapter 11, the spindle consists of both kinetochore microtubules, which are attached to the chromosomes, and polar microtubules, which overlap with one another in the center of the cell. In addition, short astral microtubules radiate outward from the centrosomes toward the cell periphery.top link
Proteolysis and the Inactivation of MPF: Anaphase and Telophase

As discussed earlier in this chapter, an important cell cycle checkpoint monitors the alignment of chromosomes on the metaphase spindle. Once 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 7.39) called the anaphase-promoting complex. 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 about 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 not catalyzed directly by the anaphase-promoting complex, which instead degrades a regulatory protein called Pds1. Degradation of Pds1 in turn 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 14.29). The separation of chromosomes during anaphase then 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).

The other key regulatory protein targeted for ubiquitination and degradation by the anaphase-promoting complex is cyclin B. Degradation of cyclin B leads to inactivation of MPF, which is required for the cell to exit mitosis and return to interphase. Many of the cellular changes involved in these transitions are simply the reversal of the events induced by MPF during entry into mitosis. For example, reassembly of the nuclear envelope, chromatin decondensation, and the return of microtubules to an interphase state probably result directly from loss of MPF activity and dephosphorylation of proteins that had been phosphorylated by MPF at the beginning of mitosis. As discussed next, inactivation of MPF also triggers cytokinesis.top link
Cytokinesis

The completion of mitosis is usually accompanied by cytokinesis, giving rise to two daughter cells. Cytokinesis usually initiates in late anaphase and is triggered by the inactivation of MPF, thereby coordinating nuclear and cytoplasmic division of the cell. As discussed in Chapter 11, cytokinesis of animal cells is mediated by a contractile ring of actin and myosin II filaments that forms beneath the plasma membrane (Figure 14.30). The location of this ring is determined by the position of the mitotic spindle, so the cell is eventually cleaved in a plane that passes through the metaphase plate perpendicular to the spindle. Cleavage proceeds as contraction of the actin-myosin filaments pulls the plasma membrane inward, eventually pinching the cell in half.

The mechanism of cytokinesis is different for higher plant cells, which are surrounded by rigid cell walls. Rather than being pinched in half by a contractile ring, these cells divide 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 apparatus associate with spindle microtubules and accumulate at the former site of the metaphase plate. These vesicles then fuse to form a large, 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 it reaches the plasma membrane. The membrane surrounding the cell plate then fuses with the parental plasma membrane, dividing the cell in two.top link