Practice question

Telophase reverses many mitotic changes to re-establish interphase nuclear architecture in daughter cells following sister chromatid arrival at poles. Decline in cyclin B levels due to APC/C-Cdh1 mediated proteolysis extinguishes CDK1 activity, allowing protein phosphatases PP1 recruited to kinetochores by Repo-Man and PP2A-B55 to dephosphorylate key substrates. Dephosphorylation causes dissociation of condensin I and II complexes leading to chromatin decondensation and transcriptional restart, reassembly of nuclear lamina from lamin A/C and B1/B2 depolymerized during prophase, recruitment of nucleoporins through ELYS chromatin-binding to reform nuclear pore complexes restoring nucleocytoplasmic transport, and reformation of nucleolus around nucleolar organizer regions with RNA polymerase I activity resuming rRNA synthesis. Spindle microtubules depolymerize, while central spindle transiently persists forming midbody. Decondensation restores accessibility of genome for G1 gene expression programs, completing mitotic exit concurrent with cytokinesis abscission mediated by ESCRT-III filaments. This circuitry is highly conserved across eukaryotes, integrating growth factor signals, DNA damage surveillance, and developmental cues, and its disruption frequently underlies oncogenesis, providing targets for checkpoint inhibitors and cancer therapeutics.