Practice question

When Cdc14 phosphatase activity compromised, consequence is arrest in late anaphase or telophase despite successful cohesin cleavage and initial chromosome segregation. Cdc14 normally released through FEAR and MEN pathways dephosphorylates key CDK substrates: Cdh1 converting APC/C coactivator to Cdh1 isoform leading to degradation of cyclin B, Plk1 and securin remnants, Swi5 transcription factor enabling synthesis of Sic1 stoichiometric CDK inhibitor, Cdc15 reinforcing feedback, and structural proteins Fin1, Ase1, Ask1 promoting spindle stability reversal. Inhibition via genetic deletion, temperature sensitive alleles, siRNA or small molecule blocks those events. Cyclin B and remaining CDK1-Cyclin B complexes persist, mitotic phosphorylations on lamins, condensins, nucleoporins remain high, nuclear envelope fails to reform around segregated masses, chromosomes stay condensed, central spindle poorly organized and actomyosin contraction defective due to persistence of CDK phosphorylation on Iqg1 and Hof1. In animal cells PP2A-B55 partially compensates but combined loss leads to prolonged hyperphosphorylated state, impaired abscission and frequent cytokinesis failure producing binucleate tetraploid daughters predisposing to aneuploidy. 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.