Symmetry breaking in mouse oocytes requires transient F-actin meshwork destabilization
Author(s) -
Jessica Azoury,
Karen Wingman Lee,
Virginie Georget,
Pascale Hikal,
MarieHélène Verlhac
Publication year - 2011
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.060269
Subject(s) - biology , meiosis , microbiology and biotechnology , formins , prophase , spindle apparatus , actin , cell division , oocyte , cytokinesis , microtubule , actin cytoskeleton , cytoskeleton , genetics , embryo , gene , cell
Female meiotic divisions are extremely asymmetric, giving rise to a large oocyte and small degenerating polar bodies, keeping the maternal stores for further embryo development. This asymmetry is achieved via off-center positioning of the division spindle. Mouse oocytes have developed a formin-2-dependent actin-based spindle positioning mechanism that allows the meiotic spindle to migrate towards the closest cortex. Using spinning disk microscopy and FRAP analysis, we studied the changes in the organization of the cytoplasmic F-actin meshwork during the first meiotic division. It is very dense in prophase I, undergoes a significant density drop upon meiosis resumption and reforms progressively later on. This meshwork remodeling correlates with endogenous formin 2 regulation. High formin 2 levels at meiosis I entry induce meshwork maintenance, leading to equal forces being exerted on the chromosomes, preventing spindle migration. Hence, the meshwork density drop at meiosis resumption is germane to the symmetry-breaking event required for successful asymmetric meiotic divisions.
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