AP Biology Unit 4 practice questions
Try 10 multiple-choice questions from Unit 4 here. Pick an answer to see why it's right or wrong, then take the timed test above for a full AP-style set.
Question 1
A mutation prevents a cell from producing functional cyclin-dependent kinase (CDK), but cyclin proteins are still made. What effect on the cell cycle is most likely?
Cells fail to pass key checkpoints because cyclin-CDK complexes cannot phosphorylate targets
Cells speed through key checkpoints because cyclins alone can activate DNA replication proteins
Cells bypass key checkpoints because loss of CDK eliminates all checkpoint signaling proteins entirely
Cells complete normal mitosis because CDK is required only for cytokinesis, not checkpoints
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Answer: (A)
Linking checkpoint control to cyclin-CDK activity explains the disruption. Without functional CDK, cyclins cannot activate the kinase activity needed to phosphorylate proteins that drive progression through G1/S and G2/M checkpoints.
Question 2
A researcher applies a chemical that stabilizes microtubules so they cannot depolymerize during mitosis. What outcome is most likely in dividing animal cells?
Cells arrest in mitosis because sister chromatids cannot separate when spindle microtubules cannot shorten
Cells arrest in interphase because stabilized microtubules prevent DNA polymerase from copying chromosomes
Cells complete mitosis normally because chromatid separation depends only on actin filaments at the cortex
Cells skip mitosis entirely because stabilized microtubules force cyclins to degrade before G2 ends
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Answer: (A)
Connecting spindle dynamics to chromosome movement explains the arrest. If microtubules cannot depolymerize, chromatids cannot be pulled to opposite poles, activating checkpoint control and halting mitotic progression.
Question 3
In a multicellular animal, a mutation makes the G1 checkpoint nonfunctional, so cells do not pause to verify DNA damage before S phase. Which outcome is most likely over many cell divisions?
Cells accumulate mutations because damaged DNA is replicated, increasing genomic instability and cancer risk
Cells accumulate mutations because DNA repair enzymes are no longer produced in any cell type
Cells stop dividing because the nonfunctional G1 checkpoint permanently activates apoptosis in all tissues
Cells remain genetically stable because skipping G1 increases division rate but reduces mutation fixation
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Answer: (A)
Relating checkpoint failure to DNA replication explains the long-term effect. If cells enter S phase without repair, DNA lesions can become fixed as mutations, raising genomic instability and the likelihood of tumor formation.
Question 4
A tumor suppressor protein that normally triggers apoptosis when DNA damage is severe becomes nonfunctional in a cell lineage. After exposure to a mutagen that causes double-strand breaks, what is the most likely result?
Damaged cells survive and divide, allowing mutations to persist and expand within the tissue lineage
Damaged cells survive and divide, but their mutations are ALWAYS corrected during cytokinesis by enzymes
Damaged cells survive and divide, yet double-strand breaks NEVER affect gene function in any organism
Damaged cells survive and divide, because loss of apoptosis COMPLETELY prevents DNA damage from occurring
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Answer: (A)
Connecting apoptosis to quality control explains the outcome. If the apoptosis trigger is lost, cells with severe damage may avoid programmed death and continue dividing, propagating mutations through the lineage.
Question 5
A drug prevents formation of the actin-myosin contractile ring in animal cells but does not affect DNA replication or mitotic spindle function. What is the most likely immediate consequence?
Cells become multinucleate because nuclear division occurs, but cytokinesis fails to separate daughters
Cells become multinucleate because the drug blocks centrosome duplication, preventing spindle formation
Cells become multinucleate because DNA replication stops in S phase, leaving chromosomes unseparated
Cells become multinucleate because the drug forces cells to skip mitosis and enter G0 permanently
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Answer: (A)
Linking the contractile ring to cytokinesis explains the result. If the spindle still separates chromosomes and nuclei reform, the cell can complete nuclear division but fail to physically divide, producing multinucleate cells.
Question 6
A researcher wants to test whether direct contact between immune cells is required for activation. T cells are exposed to antigen-presenting cells either with direct contact or separated by a membrane that lets small proteins diffuse but prevents cell-to-cell contact. What null hypothesis matches this experiment?
Separating the cells by a membrane will not change T cell activation levels
Separating the cells by a membrane will always eliminate all T cell activation
Direct contact will increase activation because antigen cannot be presented without touching
The membrane condition will increase activation because secreted signals become concentrated
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Answer: (A)
Stating a null hypothesis means predicting no difference between the contact and no-contact conditions. The membrane condition tests whether contact-dependent signaling changes activation compared with direct contact.
Question 7
A student tests whether a signaling molecule acts through a receptor on the cell surface. Cultured cells are treated with the signaling molecule alone or with the molecule plus an enzyme that cannot enter cells but degrades proteins in the culture medium. What result would support cell-surface receptor signaling?
Cells respond without the enzyme, but the response disappears when the enzyme is added
Cells respond equally with or without the enzyme, showing the ligand acts inside cells
Cells only respond when the enzyme is added, because receptors require protein cleavage
Cells show no response in either condition, proving the receptor is exclusively intracellular
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Answer: (A)
Predicting loss of response when an extracellular enzyme degrades the ligand supports signaling that begins outside the cell. Cell-surface receptor signaling depends on the ligand being present in the medium to bind the receptor.
Question 8
A researcher tests whether cells coordinate behavior through gap junctions. Cardiac muscle cells are cultured in a sheet and normally contract in synchrony. The researcher adds a chemical that blocks gap junction channels but does not kill the cells. What result should be predicted if gap junctions are required for coordination?
Cells continue contracting but lose synchrony because ions cannot pass between neighbors
Cells immediately stop contracting because gap junction blockers always halt ATP production
Cells become more synchronized because blocking junctions prevents conflicting signals from spreading
Cells contract in synchrony because gap junctions are only used for hormone signaling
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Answer: (A)
Gap junctions allow direct cytoplasmic communication, including ion flow that helps coordinate electrical activity. Blocking the channels should disrupt neighbor-to-neighbor signal spread, reducing synchronized contractions while not necessarily stopping contraction ability.
Question 9
Researchers studying a hereditary cancer syndrome discover that affected individuals have mutations in genes encoding cyclin-dependent kinase inhibitors. How would this mutation most likely affect cell cycle regulation?
Cells would progress through checkpoints without proper verification because inhibitory signals cannot slow CDK activity
Cells would permanently arrest at all checkpoints because CDK activity would be completely eliminated from the cell
Cells would undergo immediate lysis because CDK inhibitors are essential structural components of the plasma membrane
Cells would replicate DNA continuously without ever entering mitosis because CDK inhibitors trigger mitotic entry signals
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Answer: (A)
Connecting CDK inhibitor function to checkpoint control explains the cancer phenotype. CDK inhibitors normally halt cell cycle progression when conditions are unfavorable; without functional inhibitors, CDKs remain active and push cells through checkpoints inappropriately.
Question 10
A laboratory technician accidentally exposes cultured human fibroblasts to ultraviolet radiation during an experiment. The cells subsequently pause at the G1/S checkpoint before resuming division several hours later. What cellular process most likely occurred during this pause?
DNA repair enzymes corrected UV-induced thymine dimers before replication machinery copied the damaged template strand
Mitochondria regenerated ATP stores depleted by UV exposure before the cell had sufficient energy to proceed forward
Ribosomes synthesized entirely new chromosomes to replace those completely destroyed by the ultraviolet radiation exposure
Lysosomes digested all cellular proteins damaged by UV before the cell could safely continue through the cycle
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Answer: (A)
Applying checkpoint function to UV damage explains the observed delay. The G1/S checkpoint detects DNA damage and halts progression to allow repair enzymes to fix lesions like thymine dimers before they become permanent mutations during replication.
What's on the AP Biology Unit 4 practice test
The standard version takes about 60 minutes and follows the timing and directions of the AP exam, sized to one unit:
- 20 Multiple Choice Questions (30 minutes)
- 1 FRQ – FRQ 1 – Interpreting and Evaluating Experimental Results (Long) (15 minutes)
- 1 FRQ – FRQ 3 – Scientific Investigation (Short) (15 minutes)
Questions are drawn from 2089 multiple-choice questions and 93 FRQs written for Unit 4, Cell Communication and Cell Cycle.
Practice AP Biology Unit 4 FRQs
Answer the unit's free-response questions one at a time and get a score on every part.
- FRQ 1 – Interpreting and Evaluating Experimental Results (Long) (12 questions)
- FRQ 2 – Interpreting and Evaluating Experimental Results with Graphing (Long) (12 questions)
- FRQ 3 – Scientific Investigation (Short) (17 questions)
- FRQ 4 – Conceptual Analysis (Short) (15 questions)
- FRQ 5 – Analyze Model or Visual Representation (Short) (21 questions)
- FRQ 6 – Analyze Data (Short) (16 questions)
Review Unit 4 before you start
- 4.1 Cell Communication
- 4.2 Introduction to Signal Transduction
- 4.3 Signal Transduction Pathways
- 4.4 Feedback
- 4.5 Cell Cycle
- 4.6 Regulation of the Cell Cycle
- Regulation of the Cell Cycle Review