Cell cycle regulation (cyclins, checkpoints) Transitional Reasoning Download PDF

Questions

1. 1.

   A research team studying cell cycle checkpoints treats cultured mammalian cells with a synthetic agent that selectively prevents the proteasomal degradation of M-cyclin (cyclin B). Although the treated cells replicate their DNA normally and achieve proper chromosome alignment at the metaphase plate, they arrest indefinitely after sister chromatids have pulled apart, failing to decondense their chromosomes or reform the nuclear envelope. Based on these observations and mechanisms of cell cycle control, which deduction best explains this arrest?

   • A) Failure to degrade M-cyclin keeps the spindle assembly checkpoint permanently active, thereby blocking the activation of separase.
   • B) Constant M-cyclin levels stimulate premature DNA re-replication, which arrests the cell cycle before spindle disassembly can begin.
   • C) Continued activity of the cyclin–cyclin-dependent kinase complex prevents the dephosphorylation of target proteins required for mitotic exit.
   • D) Unscheduled accumulation of M-cyclin directly inhibits the anaphase-promoting complex, preventing the cleavage of cohesin rings.