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formin3是果蝇中气管融合所介导的F-肌动蛋白结构组装所必需的。

Formin3 is required for assembly of the F-actin structure that mediates tracheal fusion in Drosophila.

作者信息

Tanaka Hiromasa, Takasu Etsuko, Aigaki Toshiro, Kato Kagayaki, Hayashi Shigeo, Nose Akinao

机构信息

Department of Physics, Graduate School of Science, University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.

出版信息

Dev Biol. 2004 Oct 15;274(2):413-25. doi: 10.1016/j.ydbio.2004.07.035.

DOI:10.1016/j.ydbio.2004.07.035
PMID:15385168
Abstract

During tracheal development in Drosophila, some branches join to form a continuous luminal network. Specialized cells at the branch tip, called fusion cells, extend filopodia to make contact and become doughnut shaped to allow passage of the lumen. These morphogenetic processes accompany the highly regulated cytoskeletal reorganization of fusion cells. We identified the Drosophila formin3 (form3) gene that encodes a novel formin and plays a role in tracheal fusion. Formins are a family of proteins characterized by highly conserved formin homology (FH) domains. The formin family functions in various actin-based processes, including cytokinesis and cell polarity. During embryogenesis, form3 mRNA is expressed mainly in the tracheal system. In form3 mutant embryos, the tracheal fusion does not occur at some points. This phenotype is rescued by the forced expression of form3 in the trachea. We used live imaging of GFP-moesin during tracheal fusion to show that an F-actin structure that spans the adjoining fusion cells and mediates the luminal connection does not form at abnormal anastomosis sites in form3 mutants. These results suggested that Form3 plays a role in the F-actin assembly, which is essential for cellular rearrangement during tracheal fusion.

摘要

在果蝇气管发育过程中,一些分支相互连接形成一个连续的管腔网络。分支末端的特化细胞,即融合细胞,会伸出丝状伪足进行接触,并变成甜甜圈形状,以使管腔能够通过。这些形态发生过程伴随着融合细胞中高度有序的细胞骨架重组。我们鉴定出果蝇formin3(form3)基因,它编码一种新型formin,并在气管融合中发挥作用。Formins是一类蛋白质家族,其特征在于具有高度保守的formin同源(FH)结构域。Formin家族在各种基于肌动蛋白的过程中发挥作用,包括胞质分裂和细胞极性。在胚胎发育过程中,form3 mRNA主要在气管系统中表达。在form3突变体胚胎中,气管融合在某些部位无法发生。通过在气管中强制表达form3可以挽救这种表型。我们在气管融合过程中对GFP - moesin进行实时成像,结果显示在form3突变体的异常吻合部位,跨越相邻融合细胞并介导管腔连接的F - 肌动蛋白结构无法形成。这些结果表明,Form3在F - 肌动蛋白组装中发挥作用,而F - 肌动蛋白组装对于气管融合过程中的细胞重排至关重要。

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