Practice question

Early prometaphase generates many attachment errors because kinetochores initially capture microtubules stochastically. Syntelic where both sisters attach same pole, monotelic where only one sister attached, and merotelic where one kinetochore attached to both poles often arise. These erroneous configurations lack balanced tension between sister centromeres. Aurora B kinase, as catalytic component of chromosomal passenger complex concentrated at inner centromere between sisters, senses low tension via proximity gradient. Active when kinetochores are close, Aurora B phosphorylates N-terminal tail of Ndc80/Hec1 at multiple serines, creating negative charge weakening electrostatic interaction with acidic C-terminal tails of tubulin, phosphorylates Dam1/Ska, Knl1, and activates MCAK kinesin-13 depolymerase and stathmin destabilizing kinetochore fibers. Detached kinetochore becomes free to reattach correctly. Once amphitelic attachment generates intra-kinetochore stretch of roughly 100 nm away from inner centromere, substrates move outside Aurora B activity zone, allowing dephosphorylation by PP1 recruited via KNL1 RVXF motif and PP2A-B56 recruited by BubR1. Stabilization then occurs, enabling alignment at metaphase plate before checkpoint silencing and anaphase onset. 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.