Biology by Bradford
Unit 4: Cell Communication and Cell Cycle. Practice questions with scoring guidelines.
104 original AP-style questions on Unit 4, written to the CED learning objectives: 80 multiple-choice, 24 free-response. Below is a 20-mark practice set built from them, ready to assign as a unit check or homework, or to sit yourself and score against the guidelines. Print it, project it, or build a fresh one.
Topics in this unit
- 4.1 Cell Communication 13 questions
- 4.2 Introduction to Signal Transduction 30 questions
- 4.3 Signal Transduction 12 questions
- 4.4 Changes in Signal Transduction Pathways 16 questions
- 4.5 Feedback 15 questions
- 4.6 Cell Cycle 25 questions
- 4.7 Regulation of Cell Cycle 6 questions
In the bank for Unit 4
- 80 multiple-choice
- 24 free-response
Every question is original and tagged to a learning objective and science practice.
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The practice set
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Researchers investigate a signal transduction pathway that controls cell division in a cultured animal cell line. Growth factor GF binds to receptor R on the cell surface, which activates an intracellular kinase cascade that promotes cell division. The researchers measured the rate of cell division (cell divisions per hour per 1,000 cells) under several conditions, shown in the table.
The result obtained when the receptor-blocking antibody is added together with growth factor GF best supports which conclusion?
| Condition | Cell divisions per hour per 1,000 cells |
|---|---|
| Normal cells + GF | 8 |
| Normal cells, no GF | 1 |
| Normal cells + GF + receptor-blocking antibody | 1 |
| Normal cells + GF + kinase inhibitor | 2 |
| Mutant cells (receptor R always active), no GF | 7 |
- GF triggers cell division without needing to bind receptor R.
- GF must bind receptor R to trigger the cell-division response.
- The kinase cascade acts on the signal before the receptor does.
- GF functions as an intracellular second messenger.
On a hot day, a person's core body temperature begins to rise. The hypothalamus responds by triggering sweating and widening of the skin blood vessels, which increase heat loss and bring body temperature back down toward its normal value. Which term best describes this mechanism, and why?
- Positive feedback, amplifying the rise
- No feedback, temperature is unregulated
- Negative feedback, opposing the change
- Positive feedback, both rising together
When exposed to gradually falling temperatures in autumn, many plants detect the cold and activate signaling pathways that switch on genes encoding protective proteins and antifreeze compounds, increasing their tolerance to freezing. Which statement best describes the role of the environment in this response?
- Cold is detected and alters gene expression
- Cold permanently prevents gene expression
- The plant responds without any external cue
- The genes are expressed at the same level
In a certain cell, an extracellular signaling molecule (ligand L) binds a membrane receptor. The activated receptor switches on enzyme E, which produces a second messenger (M). Molecule M activates protein kinase K, which triggers the cellular response: secretion of product P. In addition, kinase K activates an enzyme that breaks down M. The pathway can be summarized as: Ligand L → Receptor → Enzyme E → second messenger M → Kinase K → Response (secretion of P), with kinase K also promoting the breakdown of M.
The following information applies to part A.
Progression through the eukaryotic cell cycle is controlled by cyclin–cyclin-dependent kinase (cyclin–CDK) complexes and by internal checkpoints. The G1 checkpoint determines whether a cell proceeds into S phase.
The following information applies to parts B, C, and D.
The following information applies to parts B, C, and D. Researchers studied a checkpoint protein, CP, in cultured mammalian cells. Wild-type (WT) cells and cells carrying a loss-of-function mutation in the CP gene (CP⁻) were either left untreated or exposed to a dose of ultraviolet (UV) light that damages DNA. Six hours later the percentage of cells in each phase of the cell cycle was determined (Table 1; mean of three replicate cultures, SE x̄ ≤ 2 percentage points for every value).
| Cell line | Treatment | Cells in G1 (%) | Cells in S (%) | Cells in G2/M (%) |
|---|---|---|---|---|
| WT | No UV | 45 | 30 | 25 |
| WT | UV | 78 | 8 | 14 |
| CP⁻ | No UV | 44 | 31 | 25 |
| CP⁻ | UV | 43 | 32 | 25 |
The following information applies to parts C and D.
In the same cells, the researchers measured the activity of the G1/S cyclin–CDK complex six hours after UV exposure, expressed relative to the activity in untreated cells of the same line (Table 2).
| Cell line | Relative G1/S cyclin–CDK activity after UV (untreated = 1.00) ± SE x̄ |
|---|---|
| WT | 0.20 ± 0.03 |
| CP⁻ | 0.95 ± 0.06 |
Strain L-7 is a marine bacterium that emits light (bioluminescence), but only when a culture reaches a high population density; sparse cultures do not glow, even though the cells are healthy. Researchers propose that L-7 cells continuously release a small signaling molecule into the surrounding medium and that luminescence is switched on when the concentration of the molecule exceeds a threshold, which happens only when many cells share the same volume of medium. The researchers can grow L-7 to any density, remove cells from a culture by filtration to obtain cell-free medium, and measure the light emitted per cell.
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Each point is worth 1 point and is credited independently. Accept any one of the listed alternatives per point; ( ) marks optional wording and / separates interchangeable wording.
- B — Blocking the receptor drops division to baseline even with GF present, showing GF must bind receptor R to start the response.
- C — The response (heat loss) counteracts the initial rise in temperature and restores it toward the set point, which is negative feedback.
- A — The external cue of cold is detected and initiates a signaling pathway that changes gene expression and increases freezing tolerance.
- M is the second messenger; it relays and amplifies the signal inside the cell to activate kinase K.
- Molecule M; it carries the signal from enzyme E to kinase K within the cell.
Total for part (A): 1 point
- The activated kinase reduces the level of M, which lowers its own activation and limits the response.
- K decreases M, turning down the pathway that activated K, so the response inhibits its own signal.
Total for part (B): 1 point
- Secretion of P would increase and stay elevated rather than shutting off.
- P would be secreted at higher, sustained levels because M is not removed.
Total for part (C): 1 point
- Without breakdown of M, the negative feedback that normally lowers M is lost, so M and kinase K stay active and keep driving secretion of P.
- The feedback that shuts the pathway off is removed, so M persists, K remains on, and P continues to be produced.
Total for part (D): 1 point
Total for question 4: 4 points
- Cyclin–CDK complexes phosphorylate target proteins that trigger the transition from one phase to the next (e.g., G1 to S, G2 to M); their activity rises and falls as cyclin levels change.
- A cyclin must bind its CDK to activate the kinase; the active complex drives the cell past a checkpoint into the next phase.
- At the G1 checkpoint the cell monitors DNA for damage (and checks cell size/growth signals); if damage is detected the cycle is halted before S phase so DNA is not replicated with errors, allowing repair or, if repair fails, apoptosis.
- Arresting damaged cells in G1 prevents mutations from being copied and passed on to daughter cells.
Total for part (A): 2 points
- They serve as controls showing the normal cell-cycle distribution of each cell line, so any change can be attributed to the UV treatment rather than to the cell line itself.
- A negative control/baseline for comparison with the UV-treated cultures.
- UV increased the percentage of WT cells in G1 (45% to 78%) and decreased the percentages in S (30% to 8%) and G2/M (25% to 14%).
- After UV, WT cells accumulated in G1 and far fewer entered S phase.
- A greater percentage of CP⁻ daughter cells than WT daughter cells would carry chromosomal abnormalities.
- CP⁻ cells would produce more abnormal daughter cells than WT cells.
Total for part (B): 3 points
- After UV, CP⁻ cells did not arrest in G1 (43% G1, 32% S, essentially the same as untreated) and their G1/S cyclin–CDK activity stayed at 0.95, so they replicated and divided damaged DNA; WT cells arrested (78% G1) with cyclin–CDK activity reduced to 0.20, giving time for repair before division.
- CP is needed to inhibit G1/S cyclin–CDK and halt the cycle after DNA damage (Table 2: 0.20 in WT vs 0.95 in CP⁻); without arrest, CP⁻ cells continue through S and M with unrepaired damage, producing abnormal chromosomes.
- Expose CP⁻ cells to UV and treat half of them with a drug that inhibits G1/S CDK activity, leaving the other half untreated (control); measure the percentage of cells in G1 (or the percentage of abnormal daughter cells); if the hypothesis is correct, drug-treated CP⁻ cells should arrest in G1 (and produce fewer abnormal daughters) like WT cells.
- Introduce a functional CP gene into CP⁻ cells (rescue) versus an empty vector (control), expose both to UV, and measure G1/S cyclin–CDK activity and G1 arrest; rescued cells should show reduced CDK activity and G1 accumulation.
Total for part (C): 2 points
- Without the checkpoint, cells with damaged DNA continue to divide, so mutations (including mutations in other genes controlling growth) accumulate and are passed to daughter cells, leading to uncontrolled division and tumor formation.
- Loss of cell-cycle control removes a brake on division; cells divide when they should not and accumulate further mutations, a hallmark of cancer.
- The data support the claim only for cells with no induced DNA damage (44/31/25 vs 45/30/25); CP clearly acts when DNA is damaged, and because spontaneous DNA damage occurs in every normal cycle, CP likely has a role even without UV that this experiment (six hours, one measurement) was not designed to detect.
- Partly supported: the untreated distributions are the same, so CP does not control routine progression; but the UV data show that CP is essential for the damage response, so the claim overstates the conclusion.
Total for part (D): 2 points
Total for question 5: 9 points
- If luminescence is triggered by a secreted signaling molecule, then adding cell-free medium from a dense culture to a sparse culture will cause the sparse culture to emit light, even though its cell density remains low.
- A sparse culture that receives filtered medium from a dense, glowing culture will begin to glow, because the medium carries the accumulated signaling molecule.
Total for part (A): 1 point
- Independent variable = the type of medium added to the sparse culture (cell-free medium from a dense culture versus fresh sterile medium); dependent variable = light emitted per cell; control = a sparse culture receiving the same volume of fresh sterile medium that has never contained cells.
- IV is whether the added medium came from a dense culture, DV is luminescence per cell, and the control is sparse cells given an equal volume of fresh medium (so that dilution and handling are the same).
Total for part (B): 1 point
- Grow L-7 to high density, filter the culture to remove all cells, and add a fixed volume of this cell-free medium to several replicate sparse cultures; add the same volume of fresh sterile medium to an equal number of replicate sparse cultures; incubate all cultures identically for a set time, then measure light output and cell number in each to calculate light per cell, and compare the means of the two treatments.
- Set up replicate sparse cultures, treat half with filtered dense-culture medium and half with fresh medium, keep temperature, volume and incubation time constant, and record luminescence per cell for every culture at the same time point.
Total for part (C): 1 point
- Support: sparse cultures given cell-free medium from a dense culture emit substantially more light per cell than sparse cultures given fresh medium, which remain dark. Refute: both treatments emit little or no light, indicating that the medium from dense cultures does not carry a luminescence-inducing signal.
- If the filtered medium induces glowing while fresh medium does not, the hypothesis is supported; if there is no difference in luminescence between the two treatments, the hypothesis is refuted and high cell density itself, not a secreted molecule, may be required.
Total for part (D): 1 point
Total for question 6: 4 points
Other AP Biology units
- Unit 1 Chemistry of Life 96
- Unit 2 Cell Structure and Function 105
- Unit 3 Cellular Energetics 112
- Unit 5 Heredity 130
- Unit 6 Gene Expression and Regulation 116
- Unit 7 Natural Selection 149
- Unit 8 Ecology 131
All eight units → · IB Biology subtopics → · Open the exam maker →