NMY-2 维持细胞不对称性和细胞边界，并促进 SRC 依赖性的不对称细胞分裂。
NMY-2 maintains cellular asymmetry and cell boundaries, and promotes a SRC-dependent asymmetric cell division.
机构信息
Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
出版信息
Dev Biol. 2010 Mar 15;339(2):366-73. doi: 10.1016/j.ydbio.2009.12.041. Epub 2010 Jan 6.
Abstract
The nonmuscle myosin II NMY-2 is required for cytokinesis as well as for the establishment of zygote asymmetry during embryogenesis in Caenorhabditis elegans. Here we describe two conditional nmy-2 alleles that rapidly and reversibly inactivate the protein. We show that NMY-2 has late-cell-cycle roles in maintaining embryonic asymmetries and is also required for a surprisingly late step in the maintenance of the cytokinesis furrow. Finally, during a signaling-induced asymmetric cell division, NMY-2 is required for SRC-dependent phosphotyrosine signaling and acts in parallel with WNT-signaling to specify endoderm.
摘要
非肌肉肌球蛋白 II（NMY-2）对于有丝分裂以及胚胎发生过程中合子不对称性的建立都是必需的。在这里，我们描述了两个条件性的 nmy-2 等位基因，它们可以快速且可逆地使蛋白质失活。我们发现 NMY-2 在维持胚胎不对称性方面具有晚期细胞周期作用，并且对于维持胞质分裂沟的一个令人惊讶的晚期步骤也是必需的。最后，在信号诱导的不对称细胞分裂过程中，NMY-2 需要 SRC 依赖性磷酸酪氨酸信号传导，并与 WNT 信号传导平行作用以指定内胚层。
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