Question 1
Read this context: The cell cycle is regulated by fluctuating cyclin levels that activate CDKs at specific times. Checkpoints at G1/S and G2/M act as safeguards: the first prevents replication of damaged DNA, and the second prevents mitosis if replication is incomplete. Tumor suppressors like p53 can enforce checkpoint pauses, while proto-oncogenes promote progression when signals are appropriate. If cyclin/CDK activity becomes too high, cells may pass checkpoints inappropriately and proliferate. How do cyclin-dependent kinases (CDKs) influence cell cycle progression?
- They degrade DNA to prevent mutations before replication begins
- They phosphorylate proteins to promote progression when activated by cyclins (correct answer)
- They function only as checkpoint sensors that detect spindle attachment
- They are irrelevant when growth factors are present because signaling replaces them
Explanation: This question tests understanding of cell cycle regulation, specifically the role of cyclin-dependent kinases (CDKs) in promoting cell cycle progression. The cell cycle is regulated by fluctuating levels of cyclins that bind to and activate CDKs, which then phosphorylate target proteins to drive transitions between cell cycle phases. In this passage, CDKs are highlighted as key players activated by cyclins to promote progression, while checkpoints ensure appropriate timing and safeguards against errors. Choice B is correct because it accurately describes how CDKs, when activated by cyclins, phosphorylate proteins to facilitate cell cycle advancement. Choice A is incorrect because CDKs do not degrade DNA; that role is unrelated to their function in progression. Choice C is incorrect as CDKs are not limited to checkpoint sensing for spindle attachment but broadly regulate multiple phases. Choice D is incorrect because CDKs remain essential even with growth factors, as signaling pathways often act through cyclin/CDK complexes. To help students: Encourage mapping out cyclin-CDK complexes to specific cell cycle phases and their phosphorylation targets. Practice analyzing scenarios where CDK dysregulation leads to uncontrolled proliferation, such as in cancer.