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CDC42和Rac1调控果蝇翅盘上皮细胞中不同的肌动蛋白依赖性过程。

CDC42 and Rac1 control different actin-dependent processes in the Drosophila wing disc epithelium.

作者信息

Eaton S, Auvinen P, Luo L, Jan Y N, Simons K

机构信息

European Cell Biology Laboratory, Cell Biology Programme, Heidelberg, Germany.

出版信息

J Cell Biol. 1995 Oct;131(1):151-64. doi: 10.1083/jcb.131.1.151.

DOI:10.1083/jcb.131.1.151
PMID:7559772
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2120599/
Abstract

Cdc42 and Rac1 are members of the rho family of small guanosinetriphosphatases and are required for a diverse set of cytoskeleton-membrane interactions in different cell types. Here we show that these two proteins contribute differently to the organization of epithelial cells in the Drosophila wing imaginal disc. Drac1 is required to assemble actin at adherens junctions. Failure of adherens junction actin assembly in Drac1 dominant-negative mutants is associated with increased cell death. Dcdc42, on the other hand, is required for processes that involve polarized cell shape changes during both pupal and larval development. In the third larval instar, Dcdc42 is required for apico-basal epithelial elongation. Whereas normal wing disc epithelial cells increase in height more than twofold during the third instar, cells that express a dominant-negative version of Dcdc42 remain short and are abnormally shaped. Dcdc42 localizes to both apical and basal regions of the cell during these events, and mediates elongation, at least in part, by effecting a reorganization of the basal actin cytoskeleton. These observations suggest that a common cdc42-based mechanism may govern polarized cell shape changes in a wide variety of cell types.

摘要

Cdc42和Rac1是小GTP酶rho家族的成员,在不同细胞类型中,多种细胞骨架与膜的相互作用都需要它们。在此我们表明,这两种蛋白质对果蝇翅成虫盘上皮细胞的组织形成有着不同的作用。Drac1是在黏着连接处组装肌动蛋白所必需的。在Drac1显性负性突变体中,黏着连接肌动蛋白组装失败与细胞死亡增加有关。另一方面,Dcdc42在蛹期和幼虫期发育过程中涉及极化细胞形状变化的过程中是必需的。在幼虫第三龄期,Dcdc42是顶-基上皮伸长所必需的。正常的翅成虫盘上皮细胞在第三龄期高度增加两倍多,而表达Dcdc42显性负性形式的细胞则保持短小且形状异常。在这些过程中,Dcdc42定位于细胞的顶端和基部区域,并至少部分地通过影响基部肌动蛋白细胞骨架的重组来介导伸长。这些观察结果表明,一种基于Cdc42的共同机制可能控制着多种细胞类型中的极化细胞形状变化。

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Loss of epithelial differentiation and gain of invasiveness correlates with tyrosine phosphorylation of the E-cadherin/beta-catenin complex in cells transformed with a temperature-sensitive v-SRC gene.上皮分化的丧失和侵袭性的增加与用温度敏感型v-SRC基因转化的细胞中E-钙黏蛋白/β-连环蛋白复合物的酪氨酸磷酸化相关。
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