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极性蛋白 PAR-2 打破线虫合子的对称性并使其极化。

Symmetry breaking and polarization of the C. elegans zygote by the polarity protein PAR-2.

机构信息

Department of Molecular Biology and Genetics, Howard Hughes Medical Institute, Center for Cell Dynamics, Johns Hopkins School of Medicine, PCTB 706, Baltimore, MD 21205, USA.

出版信息

Development. 2010 May;137(10):1669-77. doi: 10.1242/dev.045823. Epub 2010 Apr 14.

Abstract

Polarization of the C. elegans zygote is initiated by ECT-2-dependent cortical flows, which mobilize the anterior PAR proteins (PAR-3, PAR-6 and PKC-3) away from the future posterior end of the embryo marked by the sperm centrosome. Here, we demonstrate the existence of a second, parallel and redundant pathway that can polarize the zygote in the absence of ECT-2-dependent cortical flows. This second pathway depends on the polarity protein PAR-2. We show that PAR-2 localizes to the cortex nearest the sperm centrosome even in the absence of cortical flows. Once on the cortex, PAR-2 antagonizes PAR-3-dependent recruitment of myosin, creating myosin flows that transport the anterior PAR complex away from PAR-2 in a positive-feedback loop. We propose that polarity in the C. elegans zygote is initiated by redundant ECT-2- and PAR-2-dependent mechanisms that lower PAR-3 levels locally, triggering a positive-feedback loop that polarizes the entire cortex.

摘要

线虫合子的极化是由 ECT-2 依赖的皮质流引发的,这些流将前 PAR 蛋白(PAR-3、PAR-6 和 PKC-3)从由精子中心体标记的未来胚胎后端移开。在这里,我们证明了存在第二种平行且冗余的途径,可以在没有 ECT-2 依赖的皮质流的情况下使合子极化。这条第二条途径依赖于极性蛋白 PAR-2。我们表明,即使在没有皮质流的情况下,PAR-2 也会定位于靠近精子中心体的皮质。一旦在皮质上,PAR-2 就会拮抗 PAR-3 依赖性肌球蛋白募集,从而产生肌球蛋白流,将前 PAR 复合物以正反馈环的方式从 PAR-2 处运走。我们提出,线虫合子的极性是由冗余的 ECT-2 和 PAR-2 依赖机制引发的,这些机制会局部降低 PAR-3 水平,触发一个正反馈环,从而使整个皮质极化。

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