A non-muscle myosin required for embryonic polarity in Caenorhabditis elegans

A non-muscle myosin required for embryonic polarity in Caenorhabditis elegans
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DOI:
10.1038/382455a0
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发表时间:
1996-08-01
期刊:
影响因子:
64.8
通讯作者:
Kemphues, KJ
Kemphues, KJ
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Guo, S;Kemphues, KJ

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具有不同命运的子细胞可以通过本质上不对称的分裂产生。在这种分裂之前,决定细胞命运的关键因素在母细胞中不对称地定位(2,3)。在秀丽隐杆线虫中,PAR蛋白是建立胚胎极性的早期不对称分裂所必需的(4,8),并且在早期卵裂球中不对称定位(9,10),尽管其分布机制尚不清楚。在这里,我们报告了通过与PAR-1蛋白(一种假定的丝氨酸/苏氨酸蛋白激酶)的相互作用,在秀丽隐杆线虫中鉴定出非肌肉肌球蛋白II重链(命名为NMY-2)。此外,将nmy-2反义RNA注入成虫卵巢会导致胚胎分配缺陷,导致PAR蛋白定位错误。因此,我们得出结论,NMY-2是秀丽隐杆线虫胚胎中细胞极性建立所必需的。
DAUGHTER cells with distinct fates can arise through intrinsically asymmetrical divisions'. Before such divisions, factors crucial for determining cell fates become asymmetrically localized in the mother cell(2,3). In Caenorhabditis elegans, PAR proteins are required for the early asymmetrical divisions that establish embryonic polarity(4,8), and are asymmetrically localized in early blastomeres(9,10), although the mechanism of their distribution is not known. Here we report the identification in C. elegans of a nonmuscle myosin II heavy chain (designated NMY-2) by means of its interaction with the PAR-1 protein, a putative Ser/Thr protein kinase. Furthermore, injections of nmy-2 antisense RNA into ovaries of adult worms cause embryonic partitioning defects and lead to mislocalization of PAR proteins. We therefore conclude that NMY-2 is required for establishing cellular polarity in C. elegans embryos.