Institut Curie, PSL Research University, Sorbonne Université CNRS, UMR 144, Paris, France.
Institut de Recherche Saint Louis,U976 Human Immunology Pathophysiology Immunotherapy (HIPI), CytoMorpho Lab, University of Paris, INSERM, CEA, Paris, France.
Elife. 2021 Jun 3;10:e67489. doi: 10.7554/eLife.67489.
Mitotic spindle function depends on the precise regulation of microtubule dynamics and microtubule sliding. Throughout mitosis, both processes have to be orchestrated to establish and maintain spindle stability. We show that during anaphase B spindle elongation in , the sliding motor Klp9 (kinesin-6) also promotes microtubule growth in vivo. In vitro, Klp9 can enhance and dampen microtubule growth, depending on the tubulin concentration. This indicates that the motor is able to promote and block tubulin subunit incorporation into the microtubule lattice in order to set a well-defined microtubule growth velocity. Moreover, Klp9 recruitment to spindle microtubules is dependent on its dephosphorylation mediated by XMAP215/Dis1, a microtubule polymerase, creating a link between the regulation of spindle length and spindle elongation velocity. Collectively, we unravel the mechanism of anaphase B, from Klp9 recruitment to the motors dual-function in regulating microtubule sliding and microtubule growth, allowing an inherent coordination of both processes.
有丝分裂纺锤体的功能取决于微管动力学和微管滑动的精确调节。在整个有丝分裂过程中,这两个过程必须协调一致,以建立和维持纺锤体的稳定性。我们发现,在 有丝分裂后期 B 期纺锤体伸长过程中,滑动马达 Klp9(驱动蛋白-6)也在体内促进微管生长。在体外,Klp9 可以根据微管蛋白浓度增强和抑制微管生长,这表明该马达能够促进和阻止微管蛋白亚基掺入微管晶格,以设定明确的微管生长速度。此外,Klp9 向纺锤体微管的募集依赖于其由微管聚合酶 XMAP215/Dis1 介导的去磷酸化,从而在纺锤体长度的调节和纺锤体伸长速度之间建立了联系。总的来说,我们揭示了有丝分裂后期 B 期的机制,从 Klp9 的募集到马达在调节微管滑动和微管生长方面的双重功能,允许这两个过程的内在协调。