Mitotic Acetylation of Microtubules Promotes Centrosomal PLK1 Recruitment and Is Required to Maintain Bipolar Spindle Homeostasis
Type | Article | ||||||||||||
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Date | 2021-08 | ||||||||||||
Language | English | ||||||||||||
Author(s) | Rasamizafy Sylvia Fenosoa1, 2, Delsert Claude1, 2, 3, Rabeharivelo Gabriel1, 2, Cau Julien1, 4, 5, Morin Nathalie1, 2, Van Dijk Juliette1, 2 | ||||||||||||
Affiliation(s) | 1 : Univ Montpellier, F-34293 Montpellier, France. 2 : Ctr Natl Rech Sci CNRS UMR5237, 1919 Route Mende, F-34293 Montpellier, France. 3 : Inst Francais Rech Exploitat Mer, L3AS, F-34250 Palavas Les Flots, France. 4 : IGH, CNRS UMR 9002, 141 Rue Cardonille, F-34396 Montpellier, France. 5 : Montpellier Rio Imaging, F-34293 Montpellier, France. |
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Source | Cells (2073-4409) (Mdpi), 2021-08 , Vol. 10 , N. 8 , P. 1859 (22p.) | ||||||||||||
DOI | 10.3390/cells10081859 | ||||||||||||
WOS© Times Cited | 4 | ||||||||||||
Note | This article belongs to the Special Issue The Regulation of the Cell Cycle | ||||||||||||
Keyword(s) | microtubules, acetylation, acetyltransferase ATAT1, mitosis, spindle, centrosome, kinetochore, PLK1 kinase | ||||||||||||
Abstract | 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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