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首页> 外文期刊>Development >Atypical protein kinase C cooperates with PAR-3 to establish embryonic polarity in Caenorhabditis elegans.
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Atypical protein kinase C cooperates with PAR-3 to establish embryonic polarity in Caenorhabditis elegans.

机译:非典型蛋白激酶C与PAR-3合作,在Caenorhabdise秀丽隐杆线中建立胚胎极性。

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摘要

Asymmetric cell divisions, critically important to specify cell types in the development of multicellular organisms, require polarized distribution of cytoplasmic components and the proper alignment of the mitotic apparatus. In Caenorhabditis elegans, the maternally expressed protein, PAR-3, is localized to one pole of asymmetrically dividing blastomeres and is required for these asymmetric divisions. In this paper, we report that an atypical protein kinase C (PKC-3) is essential for proper asymmetric cell divisions and co-localizes with PAR-3. Embryos depleted of PKC-3 by RNA interference die showing Par-like phenotypes including defects in early asymmetric divisions and mislocalized germline-specific granules (P granules). The defective phenotypes of PKC-3-depleted embryos are similar to those exhibited by mutants for par-3 and another par gene, par-6. Direct interaction of PKC-3 with PAR-3 is shown by in vitro binding analysis. This result is reinforced by the observation that PKC-3 and PAR-3 co-localize in vivo. Furthermore, PKC-3 and PAR-3 show mutual dependence on each other and on three of the other par genes for their localization. We conclude that PKC-3 plays an indispensable role in establishing embryonic polarity through interaction with PAR-3.
机译:在多细胞生物的发展中指定细胞类型的不对称细胞分裂,要求细胞质组分的偏振分布和有丝分裂装置的适当对准。在Caenorhabditis elegans中,母体表达蛋白质,PAR-3局部地局限于一个不对称分隔的卵囊的一极,并且是这些不对称分裂所必需的。在本文中,我们报告了非典型蛋白激酶C(PKC-3)对于适当的不对称细胞部门是必不可少的,并与PAR-3共定出。胚胎通过RNA干扰模具耗尽PKC-3,显示出类似的表型表型,包括早期不对称分裂中的缺陷和错误定量的种质特异性颗粒(P颗粒)。 PKC-3耗尽的胚胎的缺陷表型类似于突变体表达的PAR-3和另一个PAR基因,PAR-6的那些。通过体外结合分析显示PKC-3与PAR-3的直接相互作用。该结果通过观察结果加强了PKC-3和PAR-3在体内共定出。此外,PKC-3和PAR-3显示相互依赖性,并在其本地化的其他情况下彼此相互依赖。我们得出结论,PKC-3通过与PAR-3相互作用来建立胚胎极性方面发挥不可或缺的作用。

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