Abstract：
:As they enter mitosis, animal cells undergo profound actin-dependent changes in shape to become round. Here we identify the Cdk1 substrate, Ect2, as a central regulator of mitotic rounding, thus uncovering a link between the cell-cycle machinery that drives mitotic entry and its accompanying actin remodeling. Ect2 is a RhoGEF that plays a well-established role in formation of the actomyosin contractile ring at mitotic exit, through the local activation of RhoA. We find that Ect2 first becomes active in prophase, when it is exported from the nucleus into the cytoplasm, activating RhoA to induce the formation of a mechanically stiff and rounded metaphase cortex. Then, at anaphase, binding to RacGAP1 at the spindle midzone repositions Ect2 to induce local actomyosin ring formation. Ect2 localization therefore defines the stage-specific changes in actin cortex organization critical for accurate cell division.
journal_name
Dev Celljournal_title
Developmental cellauthors
Matthews HK,Delabre U,Rohn JL,Guck J,Kunda P,Baum Bdoi
10.1016/j.devcel.2012.06.003subject
Has Abstractpub_date
2012-08-14 00:00:00pages
371-83issue
2eissn
1534-5807issn
1878-1551pii
S1534-5807(12)00276-6journal_volume
23pub_type
杂志文章abstract：:Orientation of cell division is a vital aspect of tissue morphogenesis and growth. Asymmetric divisions generate cell fate diversity and epithelial stratification, whereas symmetric divisions contribute to tissue growth, spreading, and elongation. Here, we describe a mechanism for positioning the spindle in symmetric ...
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