Inhibition of ectopic microtubule assembly by the kinesin-13 KLP-7MCAK prevents chromosome segregation and cytokinesis defects in oocytes [RESEARCH ARTICLE]

Emmanuelle Gigant, Marine Stefanutti, Kimberley Laband, Agata Gluszek-Kustusz, Frances Edwards, Benjamin Lacroix, Gilliane Maton, Julie C. Canman, Julie P.I. Welburn, and Julien Dumont

In most species, oocytes lack centrosomes. Accurate meiotic spindle assembly and chromosome segregation -essential to prevent miscarriage or developmental defects- thus occur through atypical mechanisms that are not well characterized. Using quantitative in vitro and in vivo functional assays in the C. elegans oocyte, we provide here novel evidence that the kinesin-13 KLP-7 promotes the destabilization of the whole cellular microtubule network. By counteracting ectopic microtubule assembly and disorganization of the microtubule network, this function is strictly required for spindle organization, chromosome segregation, and cytokinesis in meiotic cells. Strikingly, when centrosome activity was experimentally reduced, the absence of the kinesin-13 proteins KLP-7 or MCAK also resulted in ectopic microtubule asters during mitosis in C. elegans zygotes and HeLa cells, respectively. Our results highlight the general function of kinesin-13 microtubule depolymerases in preventing ectopic, spontaneous microtubule assembly, when centrosome activity is defective or absent, which otherwise leads to spindle microtubule disorganization and aneuploidy.

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