ArticleiScience2026
MCAK/Kif2C centromeric activity level tunes K-fiber turnover through distinct pathways.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
MCAK/Kif2C is a microtubule-depolymerizing kinesin implicated in the correction of chromosome attachment errors. When eliminated from kinetochores, cells exhibit delayed congression and a modest increase in chromosome missegregation. Curiously, MCAK/Kif2C overexpression (OE) promotes these same defects. Both depletion and excess levels of centromeric MCAK/Kif2C increase acetylated tubulin levels in the spindle, suggesting an increase in k-fiber stability. We conclude that this is the likely mechanism for the increase in chromosome segregation errors observed in both of these antagonistic conditions. Reduced MCAK/Kif2C increased the tubulin ratio on the two faces of the kinetochore, suggesting a greater likelihood of erroneous lateral MT interactions. In contrast, excess MCAK/Kif2C reduced the tubulin ratio at the kinetochore, stabilizing end-on MT interactions that increase the IKD and ultimately culminate in excessive stabilization of K-fiber microtubules. Both of these conditions promote chromosome segregation errors.
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