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一种古老的 Sec10 形成蛋白融合提供了对肌动蛋白介导的胞吐作用调节的见解。

An ancient Sec10-formin fusion provides insights into actin-mediated regulation of exocytosis.

机构信息

Plant Biology Graduate Program, University of Massachusetts Amherst, Amherst, MA.

Biological Sciences Department, Dartmouth College, Hanover, NH.

出版信息

J Cell Biol. 2018 Mar 5;217(3):945-957. doi: 10.1083/jcb.201705084. Epub 2018 Jan 26.

DOI:10.1083/jcb.201705084
PMID:29374070
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5839782/
Abstract

Exocytosis, facilitated by the exocyst, is fundamentally important for remodeling cell walls and membranes. Here, we analyzed , a novel gene that encodes a fusion of an exocyst subunit (Sec10) and an actin nucleation factor (formin). We showed that the fusion occurred early in moss evolution and has been retained for more than 170 million years. In , is essential, and the expressed protein is a fusion of Sec10 and formin. Reduction of For1F or actin filaments inhibits exocytosis, and For1F dynamically associates with Sec6, another exocyst subunit, in an actin-dependent manner. Complementation experiments demonstrate that constitutive expression of either half of the gene or the paralogous Sec10b rescues loss of For1F, suggesting that fusion of the two domains is not essential, consistent with findings in yeast, where formin and the exocyst are linked noncovalently. Although not essential, the fusion may have had selective advantages and provides a unique opportunity to probe actin regulation of exocytosis.

摘要

外排作用,由外泌体促进,对于重塑细胞壁和膜是至关重要的。在这里,我们分析了一个新基因,它编码了一个外泌体亚基(Sec10)和一个肌动蛋白成核因子(formin)的融合。我们表明,这种融合发生在苔藓植物进化的早期,并已经保留了超过 1.7 亿年。在中,是必需的,表达的蛋白是 Sec10 和formin 的融合。For1F 或肌动蛋白丝的减少抑制外排作用,并且 For1F 以依赖于肌动蛋白的方式与另一个外泌体亚基 Sec6 动态结合。互补实验表明,该基因或其同源 Sec10b 的一半的组成型表达可挽救 For1F 的缺失,这表明两个结构域的融合不是必需的,与酵母中的发现一致,在酵母中,formin 和外泌体通过非共价键连接。虽然不是必需的,但融合可能具有选择优势,并提供了一个独特的机会来研究肌动蛋白对胞吐作用的调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/b1e244eb3682/JCB_201705084_Fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/31247e254542/JCB_201705084_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/4c540f3b6eae/JCB_201705084_Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/9d46cd6ab82e/JCB_201705084_Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/f8821bda68f2/JCB_201705084_Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/d44cf784e567/JCB_201705084_Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/ba3005b9f8f0/JCB_201705084_Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/b1e244eb3682/JCB_201705084_Fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/31247e254542/JCB_201705084_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/4c540f3b6eae/JCB_201705084_Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/9d46cd6ab82e/JCB_201705084_Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/f8821bda68f2/JCB_201705084_Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/d44cf784e567/JCB_201705084_Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/ba3005b9f8f0/JCB_201705084_Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ad/5839782/b1e244eb3682/JCB_201705084_Fig7.jpg

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