2:28 PM Mon Jan 14 < Fo! Ha ‘The Continuity of Life: Cellular Reproduction CHAPTER? EER} meiotic cell division produces haploid cells, each containing, only one homologue of each pair of chromosomes. In a mals, these haploid cells usually become gametes. Consider again our hypothetical prey animals. A haploid sperm from animal A might contain alleles contributing to camouflage coloration, and a haploid egg from animal B might contain, alleles that favor freezing in place atthe first sign of a preda- tor. Fusion of these gametes may combine the alleles in a single animal that has both camouflage coloration and be- ‘comes motionless when a predator approaches. ‘Although mutations create new alleles, and are there- fore the ultimate source of the genetic variability upon which ‘evolution is based, the rate of mutations is very low. Com- bining useful alleles through sexual reproduction allows for, much more rapid evolution, as new combinations of alleles better adapt organisms to changing environments. CHECK YOUR LEARNING Can you describe an important advantage of sexual reproduction over asexual reproduction? 9.8 HOW DOES MEIOTIC CELL DIVISION PRODUCE HAPLOID CELLS? ‘The key to sexual reproduction in eukaryotes is meiotic cell division, in which a diploid cell with paired chromo- somes gives rise to haploid daughter cells with unpaired, chromosomes. Meiotic cell division consists of mei (the specialized nuclear division that produces haploid nuclei) followed by cytokinesis. Each daughter cell re- ceives one homologue of each pair of chromosomes, For Set @< homologous ‘chromosomes {@) Duplicated homologues brior to meiosis (diploid) € Previous (0) After meiosis (haploid) example, each diploid cell in your body contains 23 pairs of chromosomes, 46 chromosomes in all; meiotic cell divi sion produces sperm or eggs with 23 chromosomes, one. from each pair. (Fittingly, “meiosis” comes from a Greek. word meaning “to diminish.”) Many of the structures and events of meiotic cell divi- sion are similar to those of mitotic cell division. However, ‘meiotic cell division differs from mitotic cell division in sev- eral important ways. A crucial difference involves DNA repli- cation: In mitotic cell division, the parent cell undergoes one round of DNA replication followed by one nuclear division. In meiotic cell division, the parent cell undergoes a single round of DNA replication followed by two nuclear divisions, (Fig. 9-13). Thus, in meiosis, the DNA is replicated before the first division (Fig. 9-13a), but it is not replicated again between the first and second divisions. ‘The first division of meiosis (called meiosis 1) sepa: rates the pairs of homologous chromosomes and sends one homologue into each of two daughter nuclei, produc- ing two haploid nuclei. Each chromosome, however, still consists of two chromatids (Fig. 9-13b). The second divi sion (called meiosis 11) separates the chromatids into inde- pendent chromosomes and parcels one into each of two daughter nuclei. Therefore, at the end of meiosis, there are four haploid daughter nuclei, each with one copy of each homologous chromosome. Because each nucleus is usually. enclosed in a different cell, meiotic cell division normally. produces four haploid cells from a single diploid parent, cell (Fig. 9-13c). Then, when a haploid sperm fuses with a haploid egg, the resulting offspring are diploid once again (Fig. 9-14). We'll explore the stages of meiosis in more deaail in the following sections. FIGURE 9-13 Meiosis halves ‘the number of chromosomes (@) Both members of a pair of homologous chromosomes are duplicated prior to meiosis. (b) During ‘meiosis | each daughter cell receives one member af each pair of homologues. (e) During meiosis I, Sister chromatids separate into independent chromosomes, and each aughter call receives one of these chromosomes. (haptoia) Next >2:29 PM Mon Jan 14 UNIT2 Inheritance Health| Watch Fo! Ha Cancer—Running Through the Stop Signs at the Cell Cycle Checkpoints ‘The ultimate causes of most cancers are mutations —damage to DNA resulting from a variety of possible causes, including mistakes 2:29 PM Mon Jan 14 Fo! Ha ‘The Continuity of Life: Cellular Reproduction CHAPTER9 AFIGURE E9-1 A CT scan of advanced lung cancer Inwomen and in people who have never smoked, about 4% to 50% of lung cancer seems to be caused by too many receptors for epidermal growth factor or by mutated receptors that ae active teen inthe absence of EGF. like the tire-spiking strips that police sometimes use to prevent criminal fram racing through roadblocks. Chances are the call cannot plow through the G; to S checkpoint, soit will not continue through the cell cycle. where the matemal and patemal chromosomes have ex: changed parts (see Fig, 9-16). In human cells, each pair of homologues usually forms two or three chiasmata during pro- phase I. The mutual exchange of DNA between maternal and paternal chromosomes at chiasmata is called erossing over. If the chromosomes have different alleles, then crossing over ‘creates genetic recombination: the formation of new combi- nations of alleles on a chromosome. Even after the exchange of DNA, the arms of the homologues remain temporarily en- tangled at the chiasmata. This keeps the two homologues to- gether until they are pulled apart during anaphase I ‘As in mitosis, the spindle microtubules begin to as- semble outside the nucleus during prophase I. Near the end, of prophase I, the nuclear envelope breaks down and spindle microtubules invade the nuclear region, capturing the chro- ‘mosomes by attaching to their kinetochores, During Metaphase |, Paired Homologous Chromosomes Line Up at the Equator of the Cell During metaphase |, interactions between the kinetochores and the spindle microtubules move the paired homologues € Previous But what if mutation strikes the gene encoding the 1p53 protein? The resut will often be inactive pS3. Then, even ifthe cells DNA is damaged, the cell skips through the G; 40S checkpoint. Not surprisingly, about half ofall cancers— including tumors ofthe breast, lung, brain, pancreas, bladder, stomach, and colon—have mutations in the p53 gene. Cancer Treatments Why is medical science, which has conquered smallpox, measles, and a host of other diseases, having such a dificult time curing cancer? One reason is that both normal and cancerous cells use the same machinery for cell division. Most treatments that slow down the multipicaion of eancer cells do so by reducing growth factor responses, by inhibiting DNA replication, orby reinforcing the checkpoints in the cell cycle. Unfortunately, these treatments also inhibit the division cof normal cells. Essential body parts, such a the stomach, intestine, and blood cells, require continual cell division to replace worn-out or damaged cells. The side effects of traditional chemotherapy are only too well known: hairloss, nausea, and skin disorders. Effective and selective treatments for cancer must target call division only, of at least mostly, in cancerous cell ‘There are a few treatments, some available to patients and some in clinical trials, that block growth factor actions only in cells that usually don’t divide very often in adults, such as breast cells. Others inhibit certain Caks that are not very active in adults or that are active only in certain cell types (which at least reduces the side effects). Still others target mutations that are found only in specific cancer cells and net in normal cells. Unfortunately, each of these less toxic treatments is effective only on a subset of cancers. A nontoxic, universal cure forall cancers is far off, and may not even be possible. to the equator of the cell (Fig. 9-15b). Unlike in metaphase of mitosis, in which individual duplicated chromosomes line up along the equator, in metaphase I of meiosis, ho- ‘mologous pairs of duplicated chromosomes, held together by. chiasmata, line up along the equator. Which member of a pair of homologous chromosomes faces which pole of the cell is random—the matemal homologue may face “north” for some pairs and “south” for other pairs. This randomness {also called independent asortment), together with genetic re- combination caused by crossing over, is responsible for the genetic diversity of the haploid cells produced by meiosis. During Anaphase |, Homologous Chromosomes Separate Anaphase in meiosis I differs considerably from anaphase in mitosis. In anaphase of mitosis, the sister chromatids separate and move to opposite poles. In contrast, in anaphase | of ‘meiosis, the sister chromatids of each duplicated homologue remain attached to each other and move to the same pole. However, the chiasmata joining the two homologues untan Ble, allowing the homologues to separate and move to opposite poles (Fig. 9-15¢), Next >