Cell Cycle (College Board AP® Biology): Exam Questions

Cyclins and cyclin-dependent kinases (CDKs) regulate cell cycle progression through a series of checkpoints. Researchers investigated the role of the G1 checkpoint by introducing a mutation into the gene encoding the Rb (retinoblastoma) protein, a tumor suppressor that regulates passage from G1 to S phase. Table 1 shows the percentage of cells in each phase of the cell cycle in wild-type cells and Rb-mutant cells.

Table 1. Distribution of cells by cell cycle phase (%)

(i) Describe the role of the Rb protein in regulating the cell cycle.

(ii) Explain how the Rb mutation alters cell cycle progression based on the data in Table 1.

(i) Identify the dependent and independent variables in this experiment.

(ii) Identify a negative control that could be included in this experiment.

(iii) Justify the inclusion of the control you identified in (ii).

The mitotic index is a useful calculation to compare the proportion of cells actively dividing in the sample.

(i) Using the equation below, calculate the difference in mitotic index between the wild-type and mutant cells using the data provided.

Mitotic Index = (Mitotic Cells / Total Cells) x 100

(ii) Explain what the difference in mitotic index suggests about how the Rb mutation affects cell proliferation.

(i) Predict the effect of the Rb mutation on overall cell proliferation in a tissue.

(ii) Justify your prediction using biological reasoning.

Mitotic index is a measure of how many cells in a population are undergoing mitosis at a given time. It is often used to estimate rates of cell division. A student designs an experiment to determine whether environmental conditions affect the rate of root growth and cell division in onion root tips.

They set up two groups of onion bulbs:

• Group A: grown in nutrient-rich water

• Group B: grown in nutrient-poor water

After 7 days, they prepare microscope slides of root tips from both groups. For each root, they count the number of cells in mitosis and the total number of cells in a defined field of view.

Describe the process of mitosis in a eukaryotic cell.

Identify the independent variable in this experiment.

Predict how the mitotic index in Group A compares to that in Group B from part (a).

Justify your prediction in part (c).

Figure 1 represents the stages of the cell cycle.

Describe the key events that occur during stage I.

Explain the role of enzymes at the checkpoint after stage I to ensure accurate transmission of genetic material into stage P.

Using Figure 1 as a template, draw an"X" to show where genetically identical daughter cells are produced.

Explain why mitotic activity increases with temperature.

Colorectal cancer (CRC) is often associated with dysregulation of genes that control apoptosis. Scientists compared the expression of several apoptosis-related genes in normal colon cells and CRC tissue. Table 1 summarizes their findings.

Table 1. The level of expression of several genes in CRC tissue in comparison to normal cells.

(i) Describe how apoptosis maintains healthy tissue in living organisms.

(ii) The information in Table 1 indicates that the product of gene RGS16 suppresses cellular signals that would otherwise trigger apoptosis.

Describe how the product of a gene could suppress a cellular signal.

The scientists also measured apoptosis rates in normal and cancerous colon tissues; these results are shown in Table 2.

Table 2. Apoptosis rates in different tissue types.

(i) Identify a suitable null hypothesis for this part of the study.

(ii) Describe how the scientists might determine whether or not to accept the null hypothesis.

(iii) State the independent and dependent variables.

A student considered the data in Table 1 and Table 2 and concluded that tumors develop due to a reduction in apoptosis.

Use the data to evaluate this conclusion.

The gene MAD2L1 is involved with regulating the onset of anaphase. Its product prevents abnormal cells from passing a mitotic checkpoint.

(i) Table 1 shows that expression of MAD2L1 is upregulated in CRC tissue. Predict the likely effect of upregulation of MAD2L1 on the cells in CRC tissue.

(ii) State why your prediction in (i) is surprising in cancer tissue.

Interactions between cyclins and cyclin-dependent kinases (CDKs) regulate progression through the stages of the cell cycle. Cyclins are regulatory proteins, while CDKs are enzymes that are only active when bound to a cyclin. Different cyclin–CDK complexes form at specific checkpoints—such as G1/S and G2/M—and promote the transitions between phases of the cell cycle by phosphorylating target proteins.

Pancreatic ductal adenocarcinoma (PDAC) is a pancreatic cancer. In many PDAC cases the tumor suppressor gene TP53 is mutated; Figure 1 below shows how the protein p53, encoded by a wild-type TP53 gene, functions inside cells lining the pancreatic duct.

(i) Explain the role of cell cycle checkpoints.

(ii) Use Figure 1 to describe the role of p53 protein in a healthy cell.

(iii) Use Figure 1 to predict the effect of a mutation in the TP53 gene that results in expression of non-functional p53 protein.

Researchers are investigating whether inhibition of CDK1 could arrest cancer cells at the G2/M checkpoint and potentially lead to apoptosis.

A research team treated two PDAC cell lines, line A (with wild-type TP53) and line B (with mutated TP53), with either a control solution or a CDK1 inhibitor. After 24 hours, they measured the percentage of cells in the G2/M phase. Their results are shown in Table 1.

Table 1. % cells in G2/M phase of different treatment groups.

Construct a graph that represents the data shown in Table 1.

(i) Describe the effect of the CDK1 inhibitor on G2/M phase accumulation in the two cell lines.

(ii) Use data in Table 1 to evaluate the claim that CDK1 inhibition is effective at regulating the cell cycle in cells with mutated TP53.

Predict how the use of a CDK1 inhibitor might affect the overall proliferation of PDAC tumors in patients.

In multicellular organisms many differentiated cells exit the active cell cycle and enter a quiescent G₀ phase. For example, neurons typically remain permanently in G₀ after development to maintain stable neural networks. In contrast, other differentiated cells—such as hepatocytes in the liver—can remain in G₀ under normal conditions, but re-enter the cell cycle in response to certain stimuli.

Genes known as Sonic Hedgehog (SHH) and Indian Hedgehog (IHH) code for Hedgehog (Hh) proteins that help start liver regeneration after injury. These proteins send signals to liver cells, encouraging them to exit G₀ phase and re-enter the cell cycle.

(i) Describe how the mitosis stage of the active cell cycle ensures genetic continuity between generations of cells.

(ii) Explain how Hh protein could function as a ligand to initiate changes within another cell.

Researchers studied the effect of inhibiting Hh signaling during liver regeneration in mice. All mice underwent 70 % partial hepatectomy (PHx) to simulate liver injury. Mice were assigned to two groups:

• Group 1: PHx + no treatment

• Group 2: PHx + treatment with cyclopamine (a Hh inhibitor)

The percentage of hepatocytes in S-phase was measured at specific time intervals using BrdU labeling. BrdU is a synthetic molecule that is chemically similar to a thymine-containing nucleotide.

Table 1. % hepatocytes in S-phase after treatment.

(i) Identify a suitable hypothesis for this experiment.

(ii) Justify the inclusion of group 1 in the study.

(iii) Explain how BrdU labeling might allow scientists to identify cells in S-phase.

(i) Describe the effect of cyclopamine on the cell cycle in mice.

(ii) Explain the possible mechanism by which cyclopamine causes the effect described in (i).

(iii) A student concluded that Hh activity is essential for liver regeneration in mice. Use data from Table 1 to evaluate this conclusion.

Regulated cell cycle re-entry is essential for tissue maintenance and regeneration. In the liver it allows for the maintenance of a specific liver-to-body weight ratio. After liver injury or partial surgical removal ( PHx), the liver undergoes regulated regeneration to restore this ratio. This self-limiting regenerative process is referred to as 'hepatostat'.

Explain how proteins like cyclopamine might aid in the maintenance of hepatostat.