Cells (Jul 2021)

Mitotic Acetylation of Microtubules Promotes Centrosomal <i>PLK1</i> Recruitment and Is Required to Maintain Bipolar Spindle Homeostasis

  • Sylvia Fenosoa Rasamizafy,
  • Claude Delsert,
  • Gabriel Rabeharivelo,
  • Julien Cau,
  • Nathalie Morin,
  • Juliette van Dijk

DOI
https://doi.org/10.3390/cells10081859
Journal volume & issue
Vol. 10, no. 8
p. 1859

Abstract

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Tubulin post-translational modifications regulate microtubule properties and functions. Mitotic spindle microtubules are highly modified. While tubulin detyrosination promotes proper mitotic progression by recruiting specific microtubule-associated proteins motors, tubulin acetylation that occurs on specific microtubule subsets during mitosis is less well understood. Here, we show that siRNA-mediated depletion of the tubulin acetyltransferase ATAT1 in epithelial cells leads to a prolonged prometaphase arrest and the formation of monopolar spindles. This results from collapse of bipolar spindles, as previously described in cells deficient for the mitotic kinase PLK1. ATAT1-depleted mitotic cells have defective recruitment of PLK1 to centrosomes, defects in centrosome maturation and thus microtubule nucleation, as well as labile microtubule-kinetochore attachments. Spindle bipolarity could be restored, in the absence of ATAT1, by stabilizing microtubule plus-ends or by increasing PLK1 activity at centrosomes, demonstrating that the phenotype is not just a consequence of lack of K-fiber stability. We propose that microtubule acetylation of K-fibers is required for a recently evidenced cross talk between centrosomes and kinetochores.

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