Practice question

Cyclin abundance oscillates generating waves of CDK activity. Cyclin D induced by mitogens drives early G1 progression, Cyclin E peaks at G1/S boundary initiating replication, then declines rapidly through SCF-Fbw7 mediated degradation after autophosphorylation. Cyclin A accumulates as cells enter and progress through S phase, reaching maximum in G2. Binding partners shift: in S phase, Cyclin A preferentially complexes with CDK2 phosphorylating components for continued DNA synthesis, E2F-dependent transcription termination, centrosome duplication and prevention of origin relicensing such as Cdc6 export. In late G2, Cyclin A switches to CDK1 phosphorylating proteins required for mitotic entry including Bora for Aurora A activation, initiating chromosome condensation, nuclear envelope breakdown priming and centrosome maturation before degradation by APC/C-Cdc20 in prometaphase after chromosome alignment begins. In comparison Cyclin B synthesizes later peaking in mitosis and Cyclin D/E function earlier. Hence S-phase associated accumulation driving replication continuation and entry into mitotic preparation characterizes Cyclin A, coordinating replication completion with preparation for segregation phases ensuring order. Additional feedback loops involving polo-like kinases, phosphatases and SCF-mediated degradation reinforce irreversibility and protect against premature progression that would compromise genome integrity and viability.