Chapter 11

1. A common signal for the initiation of binary fission is adequate nutrients.

   A-11

2. If the cell divided before DNA was fully replicated, each new cell would not receive a full complement of the genetic material, DNA.

3. In eukaryotes there is more DNA, the DNA is in numerous molecules, the DNA molecules are much larger, and the DNA is located in a separate cell compartment, the nucleus.

1. See Figure 11.3.

2. The Cdk’s are made throughout the cell cycle. However, their protein kinase active site is not available for target substrates for cell cycle activities unless a particular cyclin molecule binds to the Cdk. It is the cyclins that are made, bind to Cdk’s to activate, and then break down. The transient nature of the cyclins controls each Cdk activation in sequence at the cell cycle control points.

3. Growth factors are proteins made by cells that can travel to other cells, or act on the cells that make them, usually to stimulate cell division. Growth factors bind to specific receptors on target cells, setting off signal transduction inside the cells. This can lead to gene expression for cyclins, for example, and the cell cycle is stimulated.

4. P16 blocks the interaction of cyclin and its Cdk that act at the G1–S boundary. If there is more p16 in older people, it may mean that their cell cycle is blocked and they cannot repair damaged tissues by cell replacement.

1. A chromosome is a DNA molecule in the cell, and when the cell is in mitosis the chromosome is complexed with proteins to produce a visible, condensed structure. A chromatid is a DNA molecule complexed with proteins that is the product of S phase DNA replication. Chromatids are in pairs (the two products of replication) and lie attached to one another via the centromere until anaphase of mitosis. A daughter chromosome appears in an anaphase of mitosis, and was formerly a chromatid but has now separated from its partner as it migrated to the spindle pole.

2. During interphase, DNA is somewhat condensed by histone proteins into nucleosomes, and these fold over one another to form chromatin fibers. During prophase, the fibers attach as loops to proteins, and these in turn loop extensively to form the chromosome.

3. Chromosomes are attached to spindle microtubules, and molecular motors on the microtubules move the chromosomes along. In addition, spindle microtubules shorten from the poles, and this causes the attached chromosomes to move to the poles. Taxol prevents these processes, and so inhibits cell division. The drug also inhibits the division of normal cells that enter M phase.

4. In plant cells, a cell plate forms from Golgi vesicles and this makes a new cell wall to separate the two daughter cells. Cell membranes grow below the cell walls. In animal cells, a “purse string” of microfilaments contracts to pinch off the cell membrane, and the cells separate.

5. A nonfunctional cohesion would not allow close attachment of chromatids during cell division, and there would not be a centromere. The two chromatids would be separate and there would be no organization for kinetochore attachment. There would be ineffective segregation of one chromatid of a pair to each daughter cell.

1. Take a dividing cell and examine the chromosomes. If each chromosome differs in size and centromere placement from the others, the plant sample is haploid. If there are two copies of each chromosome, the plant is diploid.

2. Fertilization involves the union of two haploid gametes, each with one set of chromosomes, made from meiosis. So the fertilized cell is diploid.

3. All sexual life cycles have some haploid and diploid cells, fertilization, and meiosis.

4. See Figure 11.14.

1. In crossing over, there is an exchange of some genetic material between non-identical chromosomes of a pair. So the resulting chromosomes carry new combinations of genes, which can be passed on to offspring in a gamete and fertilization. In independent assortment, it is random which chromosome of a homologous pair ends up in a particular gamete. So different gametes will usually have a different set of chromosomes; that is, chromosome 1 from the father, chromosome 2 from the mother, and so on. Fertilization therefore results in diploids, each of which has a different set of chromosomes.

2. Prophase I meiosis: Chromosomes have chromatid pairs attached, and the two homologs are lined up gene for gene beside one another.

   Prophase mitosis: Chromosomes have attached chromatid pairs but are not lined up beside one another.

   Anaphase I meiosis: Homologous chromosomes, each with two attached chromatids, separate and move to the poles.

   Anaphase of mitosis: Chromatids separate and become single daughter chromosomes and move to the poles.

3. In the formation of male gametes, the X and Y chromosomes fail to separate in meiosis I anaphase. At the end of meiosis II, there will be two types of gametes: half without an X or Y, and half with X and Y. If the latter fertilizes a normal egg with a single X chromosome, the offspring will be XXY. However, if there is a similar nondisjunction in the formation of female gametes, there will be eggs with two X chromosomes. If the XX egg is fertilized by a normal, Y-containing sperm, the offspring will be XXY.

4. Polyploidy refers to an extra set or more of chromosomes (e.g., 3n instead of 2n). It arises because of failure of all chromosomes to disjoin in meiosis in gamete formation, resulting, for example, in a diploid gamete.

1. Signals for necrosis include great damage to a cell or starvation.

2. Apoptosis is necessary when cells are damaged and could be mutated, and when there are too many cells for organ structure.

3. Apoptosis is regulated by signals such as hormones and DNA damage, and a signal transduction pathway that results in apoptotic processes.

1. Normal cells: have control over cell division; stay in tissue and do not migrate. Malignant tumor cells: lose control over cell division; migrate to other places in the body. Benign tumor cells: lose control over cell division and then at some point stop dividing; do not migrate to other parts of the body.

2. In normal cells, oncogene products are not active or are made in low amounts, while in cancer cells oncogene products are made in larger amounts or mutated forms, and these act to stimulate the cell cycle. In normal cells, tumor suppressor gene products are made and are active at blocking the cell cycle. In cancer cells, tumor suppressor gene products are either mutated to be nonfunctional or are not made, and in either case are not active in blocking cell division, so cells divide and form tumors.

3. Cancer cells are not synchronous in the cell cycle. At a given point in time, some are in G1, some in S, and so on. So targeting all the phases might be better than targeting just one.

1. Labeling of the G1 nuclei in the G1/S cells was mostly complete by 16 hours.

2. The G1 control showed when DNA replication would normally occur in G1 nuclei. The G1/G1 control showed that the fusion process itself did not stimulate DNA replication; G1 cells had to be fused to S cells for DNA replication to be stimulated. Nuclei of the G1 and G1/G1 cells did not start to become labeled until about 8 hours after fusion, because these cells had to go all the way through G1 before entering S and replicating their DNA. By contrast, labeling of the G1 nuclei in the G1/S cells began soon after fusion.

3. G2 cells are further into the cell cycle than S phase cells are. It took several hours for the S phase cells to pass through S and G2 to begin mitosis.

4. The timing of mitosis in the hybrid S/G2 cells was similar to that in the unfused S cells and the S/S hybrids. This result indicates that G2 cells cannot stimulate mitosis of nuclei that are still in S phase.

1. Cells would halt at various points in the cell cycle:

   Extract 1: cells would accumulate in G2.

   Extract 2: cell would accumulate in M.

   Extract 3: cells would accumulate in G1.

   Extract 4: cells would accumulate in S.

2. Different cells in a tumor may have different errors in cell cycle control. One cell may respond to a G1 inhibitor and another cell to an S phase inhibitor.

3. The researcher could isolate compounds from each cell extract and test them individually in the same tests carried out with the extract in order to locate the specific molecule that acts as an inhibitor in each case. These molecules can be analyzed to determine their chemical structures in order to synthesize them and carry out additional tests, including animal tests, to ensure that they are safe.

4. Only one protein is overexpressed in cancer cells compared with non-cancer cells, and that protein is Cdk1, which functions at the checkpoint during mitosis. The plant extract that inhibits the cyclin B–Cdk1 complex was extract #2, and so extract #2 would be the best choice for treating this tumor.

5. Researchers would be interested in the plant extract that halted phosphatase activity but not the extract that halted kinase activity. Phosphatase activates Cdk, which leads to progression through the checkpoint. The goal of an anticancer drug is to stop progression through the checkpoint so cell division stops. Therefore it would be desirable to inhibit the phosphatase that activates Cdk. It would not be desirable to inhibit the kinase, which is already doing what is necessary to inhibit Cdk.