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

机译:皮质结构域校正可重新设置极性边界,以匹配秀丽隐杆线虫胚胎中的胞质分裂沟。

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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. Galpha-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.
机译:在不对称分裂的细胞中,无法将细胞极性与细胞分裂的部位协调起来会导致细胞命运的转变和肿瘤的发生。秀丽隐杆线虫胚胎中的细胞极性由PAR蛋白定义,PAR蛋白占据细胞皮层的一半。在非对称分裂过程中,前后PAR域之间的边界与细胞分裂的位置精确匹配,从而确保了细胞命运的完全隔离。 PAR结构域通过定位有丝分裂纺锤体来确定细胞分裂的位点,提示了一种可以协调细胞极性和细胞分裂的方法。在这里,我们报告细胞极性和细胞分裂是通过一种附加的机制进行协调的:细胞分裂的位置重新定位PAR-2边界。 Galpha介导的微管-皮质相互作用似乎将PAR-2和肌球蛋白的皮质流引向细胞分裂的位点,该细胞分裂充当PAR-2和肌球蛋白的沉陷。 PAR-2边界校正中有缺陷的胚胎会发生皮质极性和细胞质决定簇的错误分离,提示PAR域校正可能有助于阻止细胞命运的转变。

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