Abstract
Cell mechanics control the outcome of cell division. In mitosis, external forces applied on a stiff cortex direct spindle orientation and morphogenesis. During oocyte meiosis on the contrary, spindle positioning depends on cortex softening. How changes in cortical organization induce cortex softening has not yet been addressed. Furthermore, the range of tension that allows spindle migration remains unknown. Here, using artificial manipulation of mouse oocyte cortex as well as theoretical modelling, we show that cortical tension has to be tightly regulated to allow off-center spindle positioning: a too low or too high cortical tension both lead to unsuccessful spindle migration. We demonstrate that the decrease in cortical tension required for spindle positioning is fine-tuned by a branched F-actin network that triggers the delocalization of myosin-II from the cortex, which sheds new light on the interplay between actin network architecture and cortex tension.
Highlights
Cell mechanics control the outcome of cell division
Spindle positioning in Meiosis I instead depends on the progressive assembly of two actin networks: a cytoplasmic meshwork nucleated by Formin-2 and Spire1/2 together with a cortical actin thickening nucleated by the Arp2/3 complex[9]
To investigate how the regulation of cortical tension affects spindle movement to the cortex, we developed a theoretical model of spindle migration based on the following observations
Summary
Cell mechanics control the outcome of cell division. In mitosis, external forces applied on a stiff cortex direct spindle orientation and morphogenesis. In mouse oocytes on the contrary, off-center positioning of the spindle following its migration, required to allow the asymmetry in size of the first meiotic division, depends on a reduced cortical tension which is correlated with both increased cortical actin nucleation and myosin-II delocalization from the cell cortex[9]. A MAPKKK (MAP Kinase Kinase Kinase) expressed in oocytes after NEBD and activating MAPKs around 3 h after NEBD10,21,22 controls both the nucleation of this actin thickening and the removal of myosinII from the cortex, two events responsible for the drop in cortical tension required for spindle migration[9,23]. Using mathematical modelling and cortical tension manipulation, we show that cortical tension is strictly gated to allow spindle migration and that the decrease in cortical tension is mediated by F-actin dependent myosin-II exclusion from the cortex
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