Suppr超能文献

MOM-5卷曲蛋白调节DSH-2的分布以控制秀丽隐杆线虫的不对称神经母细胞分裂。

MOM-5 frizzled regulates the distribution of DSH-2 to control C. elegans asymmetric neuroblast divisions.

作者信息

Hawkins Nancy C, Ellis Gregory C, Bowerman Bruce, Garriga Gian

机构信息

Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3204, USA.

出版信息

Dev Biol. 2005 Aug 1;284(1):246-59. doi: 10.1016/j.ydbio.2005.05.024.

Abstract

Asymmetric cell divisions produce all 302 neurons of the C. elegans hermaphrodite. Here, we describe a role for a C. elegans Dishevelled homolog, DSH-2, in an asymmetric neuroblast division. In dsh-2 mutants, neurons normally descended from the anterior neuroblast daughter of the ABpl/rpppa blast cell were frequently duplicated, while non-neuronal cells produced by the posterior daughter cell were often missing. These observations indicate that in the absence of dsh-2 function, the posterior daughter cell was transformed into a second anterior-like cell. Loss of mom-5, a C. elegans frizzled homolog, produced a similar phenotype. We also show that the DSH-2 protein localized to the cell cortex in most cells of the embryo. In the absence of MOM-5/Fz, DSH-2 was localized to the cytoplasm, suggesting that MOM-5 regulates asymmetric cell division by controlling the localization of DSH-2. Although all neurons in C. elegans are produced by an invariant pattern of cell divisions, our results indicate that cell signaling may contribute to asymmetric neuroblast division during embryogenesis.

摘要

不对称细胞分裂产生了秀丽隐杆线虫雌雄同体的所有302个神经元。在此,我们描述了秀丽隐杆线虫Dishevelled同源物DSH-2在不对称神经母细胞分裂中的作用。在dsh-2突变体中,通常由ABpl/rpppa母细胞的前神经母细胞子代产生的神经元经常重复出现,而后代细胞产生的非神经元细胞常常缺失。这些观察结果表明,在缺乏dsh-2功能的情况下,后子代细胞转变为第二个类似前体细胞。秀丽隐杆线虫卷曲蛋白同源物mom-5的缺失产生了类似的表型。我们还表明,DSH-2蛋白定位于胚胎大多数细胞的细胞皮层。在没有MOM-5/Fz的情况下,DSH-2定位于细胞质中,这表明MOM-5通过控制DSH-2的定位来调节不对称细胞分裂。尽管秀丽隐杆线虫中的所有神经元都是由不变的细胞分裂模式产生的,但我们的结果表明,细胞信号传导可能在胚胎发育过程中促进不对称神经母细胞分裂。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验