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

• Main Authors: Sylvia Fenosoa Rasamizafy, Claude Delsert, Gabriel Rabeharivelo, Julien Cau, Nathalie Morin, Juliette van Dijk
• Format: Article
• Language: English
• Published: MDPI AG 2021-07-01
• Series: Cells
• Subjects: microtubules; acetylation; acetyltransferase <i>ATAT1</i>; mitosis; spindle; centrosome
• Online Access: https://www.mdpi.com/2073-4409/10/8/1859

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 <i>ATAT1</i> 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 <i>PLK1</i>. <i>ATAT1</i>-depleted mitotic cells have defective recruitment of <i>PLK1</i> 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 <i>ATAT1</i>, by stabilizing microtubule plus-ends or by increasing <i>PLK1</i> 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.