...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Mechanisms of Development >Slingshot cofilin phosphatase localization is regulated by Receptor Tyrosine Kinases and regulates cytoskeletal structure in the developing Drosophila eye
【24h】

Slingshot cofilin phosphatase localization is regulated by Receptor Tyrosine Kinases and regulates cytoskeletal structure in the developing Drosophila eye

机译：弹弓cofilin磷酸酶的定位受受体酪氨酸激酶的调节，并调节果蝇眼中发育的细胞骨架结构

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Animal development requires that positional information act on the genome to control cell fate and cell shape. The primary determinant of animal cell shape is the cytoskeleton and thus the mechanisms by which extracellular signals influence the cytoskeleton are crucial for morphogenesis. In the developing Drosophila compound eye, localized polymerization of actin functions to constrict the apical surface of epithelial cells, both at the morphogenetic furrow and later to maintain the coherence of the nascent ommatidia. As elsewhere, actin polymerization in the developing eye is regulated by ADF/cofilin ('Twinstar', or 'Tsr' in Drosophila), which is activated by Slingshot (Ssh), a cofilin phosphatase. Here we show that Ssh does act in the developing eye to limit actin polymerization in the assembling ommatidia, but not in the morphogenetic furrow. While Ssh does control cell shape, surprisingly there are no direct or immediate consequences for cell type. Ssh protein becomes apically concentrated in cells that express elevated levels of the Sevenless (Sev) receptor-tyrosine kinase (RTK), even those which receive no ligand. We interpret this as a non-signal driven, RTK-dependent localization of Ssh to allow for locally increased actin filament turnover. We suggest that there are two modes of actin remodeling in the developing eye: a non-RTK, non-Ssh mediated mechanism in the morphogenetic furrow, and an RTK and Ssh-dependent mode during ommatidial assembly.
机译：动物的发育要求位置信息作用于基因组以控制细胞命运和细胞形状。动物细胞形状的主要决定因素是细胞骨架，因此细胞外信号影响细胞骨架的机制对于形态发生至关重要。在发育中的果蝇复眼中，肌动蛋白的局部聚合作用是在形态发生沟处并随后维持新生眼孔的连贯性，从而收缩上皮细胞的顶表面。与其他地方一样，发育中的眼睛中的肌动蛋白聚合反应受ADF / cofilin（果蝇中的“ Twinstar”或“ Tsr”）调节，而ADF / cofilin被Sfilshot（Ssh）激活，后者是一种cofilin磷酸酶。在这里，我们显示Ssh确实在发育中的眼睛中起作用，以限制组装的眼睑中的肌动蛋白聚合，但不在形态发生沟中。尽管Ssh确实控制细胞的形状，但令人惊讶的是，细胞类型没有直接或直接的后果。 Ssh蛋白逐渐集中在表达高水平的Sevenless（Sev）受体酪氨酸激酶（RTK）的细胞中，即使那些没有配体的细胞也是如此。我们将其解释为Ssh的非信号驱动，RTK依赖性定位，以允许局部增加的肌动蛋白丝周转率。我们建议在发育中的眼中有两种肌动蛋白重塑模式：形态发生犁沟中的非RTK，非Ssh介导的机制，以及在成虫组装过程中的RTK和Ssh依赖性模式。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号