Cortical domain correction repositions the polarity boundary to match the cytokinesis furrow in C. elegans embryos

被引:37
作者
Schenk, Christian [1 ]
Bringmann, Henrik [2 ,3 ,4 ]
Hyman, Anthony A. [2 ]
Cowan, Carrie R. [1 ,2 ]
机构
[1] Res Inst Mol Pathol, A-1030 Vienna, Austria
[2] Max Planck Inst Mol Cell Biol & Genet, D-01309 Dresden, Germany
[3] MRC, Mol Biol Lab, Div Cell Biol, Cambridge CB2 0QH, England
[4] Max Planck Inst Biophys Chem, D-37077 Gottingen, Germany
来源
DEVELOPMENT | 2010年 / 137卷 / 10期
关键词
PAR polarity; Asymmetric cell division; Cytokinesis; C; elegans; ASYMMETRIC CELL-DIVISION; CAENORHABDITIS-ELEGANS; SPINDLE ORIENTATION; PLANAR DIVISIONS; PROTEINS RGA-3; GENES; PROGENITORS; MECHANISMS; ENCODES; EMBRYOGENESIS;
D O I
10.1242/dev.040436
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
In asymmetrically dividing cells, a failure to coordinate cell polarity with the site of cell division can lead to cell fate transformations and tumorigenesis. Cell polarity in C. elegans embryos is defined by PAR proteins, which occupy reciprocal halves of the cell cortex. During asymmetric division, the boundary between the anterior and posterior PAR domains precisely matches the site of cell division, ensuring exclusive segregation of cell fate. The PAR domains determine the site of cell division by positioning the mitotic spindle, suggesting one means by which cell polarity and cell division might be coordinated. Here, we report that cell polarity and cell division are coordinated through an additional mechanism: the site of cell division repositions the PAR-2 boundary. G alpha-mediated microtubule-cortex interactions appear to direct cortical flows of PAR-2 and myosin toward the site of cell division, which acts as a PAR-2 and myosin sink. Embryos with defects in PAR-2 boundary correction undergo mis-segregation of cortical polarity and cytoplasmic determinants, suggesting that PAR domain correction might help prevent cell fate transformation.
引用
收藏
页码:1743 / 1753
页数:11
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