FN Archimer Export Format PT J TI Mitotic Acetylation of Microtubules Promotes Centrosomal PLK1 Recruitment and Is Required to Maintain Bipolar Spindle Homeostasis BT AF RASAMIZAFY, Sylvia Fenosoa DELSERT, Claude RABEHARIVELO, Gabriel CAU, Julien MORIN, Nathalie VAN DIJK, Juliette AS 1:1,2;2:1,2,3;3:1,2;4:1,4,5;5:1,2;6:1,2; FF 1:;2:PDG-RBE-MARBEC-LAAAS;3:;4:;5:;6:; C1 Univ Montpellier, F-34293 Montpellier, France. Ctr Natl Rech Sci CNRS UMR5237, 1919 Route Mende, F-34293 Montpellier, France. Inst Francais Rech Exploitat Mer, L3AS, F-34250 Palavas Les Flots, France. IGH, CNRS UMR 9002, 141 Rue Cardonille, F-34396 Montpellier, France. Montpellier Rio Imaging, F-34293 Montpellier, France. C2 UNIV MONTPELLIER, FRANCE CNRS, FRANCE IFREMER, FRANCE CNRS, FRANCE MONTPELLIER RIO IMAGING, FRANCE SI MONTPELLIER SE PDG-RBE-MARBEC-LAAAS IN WOS Ifremer UPR DOAJ copubli-france copubli-univ-france IF 7.666 TC 4 UR https://archimer.ifremer.fr/doc/00720/83156/88048.pdf https://archimer.ifremer.fr/doc/00720/83156/88049.zip LA English DT Article DE ;microtubules;acetylation;acetyltransferase ATAT1;mitosis;spindle;centrosome;kinetochore;PLK1 kinase AB 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. PY 2021 PD AUG SO Cells SN 2073-4409 PU Mdpi VL 10 IS 8 UT 000688957100001 DI 10.3390/cells10081859 ID 83156 ER EF