Practice question

MPF converts interphase architecture into mitotic state through phosphorylation of hundreds of substrates. Nuclear entry of CDK1-Cyclin B, facilitated by phosphorylation of Cyclin B cytoplasmic retention sequence, allows access to chromatin proteins. Condensin I and II pentameric complexes containing SMC2, SMC4 become phosphorylated at non-SMC subunits CAP-D2, D3, CAP-G, H2, activating ATP-dependent loop extrusion that folds 10nm fiber into 700 nm wide rod chromosomes. Lamins phosphorylated at Ser22 Ser392 disassemble intermediate filament meshwork leading to nuclear envelope breakdown and merging with endoplasmic reticulum. Golgi matrix proteins GRASP65 GM130 phosphorylated causing vesiculation and partitioning. Interphase microtubule array destabilized while centrosomal gamma-TuRC recruitment of pericentrin enhanced drives bipolar spindle formation after Eg5 kinesin activation and NuMA dynein redistribution. Transcription inhibition through TFIIH and TFIID phosphorylation silences gene expression. Together these modifications reconfigure cell for chromosome capture, alignment and segregation, all attributable to single CDK1-Cyclin B holoenzyme activity rising at mitotic onset and falling after anaphase due to cyclin B destruction. 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.