MCAK/Kif2C centromeric activity level tunes K-fiber stability.

ABSTRACT: MCAK/Kif2C is a microtubule-depolymerizing kinesin that is implicated in the correction of chromosome attachment errors. When this protein is eliminated from kinetochores, cells exhibit delayed congression and a modest increase in chromosome mis-segregation. Curiously, MCAK/Kif2C overexpression (OE) promotes these same defects. These mitotic delays are restricted to prometaphase and can be rescued by modulating MCAK/Kif2C activity solely at the centromere. Both excessive depletion and surplus levels of centromeric MCAK/Kif2C increased inter-kinetochore distances (IKDs) commensurate with an increase in acetylated tubulin in the spindle, a readout for k-fiber stability. Because both high and low levels of centromere-associated MCAK/Kif2C increased k-fiber stability, we conclude that this is

SUBMITTER: Wordeman L 

PROVIDER: S-EPMC11870468 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature