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秀丽隐杆线虫的EGL-26蛋白介导外阴细胞形态发生。

The Caenorhabditis elegans EGL-26 protein mediates vulval cell morphogenesis.

作者信息

Hanna-Rose Wendy, Han Min

机构信息

Howard Hughes Medical Institute, University of Colorado, Boulder, CO 80309, USA.

出版信息

Dev Biol. 2002 Jan 15;241(2):247-58. doi: 10.1006/dbio.2001.0514.

DOI:10.1006/dbio.2001.0514
PMID:11784109
Abstract

In screens for Caenorhabditis elegans mutants defective in vulval morphogenesis, we isolated multiple mutants in which the uterus and the vulva fail to make a functional connection, resulting in an egg-laying defective phenotype. Two of these connection of gonad defective (Cog) mutants carry alleles of the egl-26 gene. We demonstrate that vulval lineages in egl-26 mutant animals are normal, but one vulval cell, vulF, adopts an abnormal morphology. This results in formation of an abnormally thick layer of vulval tissue at the apex of the vulva and a physical blockage of the exit to the vulva from the uterus. egl-26 was cloned and is predicted to encode a novel protein. Mosaic analysis indicates that egl-26 activity is required in the primary vulval lineage for vulF morphogenesis. Expression of a functional translational fusion of EGL-26 to GFP was observed within the primary vulval lineage only in vulE, which neighbors vulF. EGL-26 is localized at the apical edge of the vulE cell. It is thus possible that vulE acts to instruct morphological changes in the neighboring cell, vulF, in an interaction mediated by EGL-26.

摘要

在筛选秀丽隐杆线虫外阴形态发生缺陷的突变体时,我们分离出多个突变体,其中子宫和外阴无法建立功能性连接,导致产卵缺陷表型。这些性腺连接缺陷(Cog)突变体中的两个携带egl-26基因的等位基因。我们证明,egl-26突变动物的外阴谱系是正常的,但一个外阴细胞vulF呈现异常形态。这导致在外阴顶端形成异常厚的外阴组织层,并从子宫到外阴的出口出现物理阻塞。egl-26被克隆,预计编码一种新型蛋白质。嵌合体分析表明,egl-26活性在初级外阴谱系中是vulF形态发生所必需的。仅在与vulF相邻的vulE中,在初级外阴谱系内观察到EGL-26与GFP的功能性翻译融合体的表达。EGL-26定位于vulE细胞的顶端边缘。因此,vulE有可能在由EGL-26介导的相互作用中指导相邻细胞vulF的形态变化。

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