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细胞极性蛋白 Spa2 协调芽殖酵母分裂位点处 Chs2 的掺入。

Cell polarity protein Spa2 coordinates Chs2 incorporation at the division site in budding yeast.

机构信息

Instituto de Biomedicina y Biotecnología de Cantabria, Universidad de Cantabria, CSIC, Santander, Spain.

Departamento de Biología Molecular, Facultad de Medicina, Universidad de Cantabria, Santander, Spain.

出版信息

PLoS Genet. 2018 Mar 30;14(3):e1007299. doi: 10.1371/journal.pgen.1007299. eCollection 2018 Mar.

DOI:10.1371/journal.pgen.1007299
PMID:29601579
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5895073/
Abstract

Deposition of additional plasma membrane and cargoes during cytokinesis in eukaryotic cells must be coordinated with actomyosin ring contraction, plasma membrane ingression and extracellular matrix remodelling. The process by which the secretory pathway promotes specific incorporation of key factors into the cytokinetic machinery is poorly understood. Here, we show that cell polarity protein Spa2 interacts with actomyosin ring components during cytokinesis. Spa2 directly binds to cytokinetic factors Cyk3 and Hof1. The lethal effects of deleting the SPA2 gene in the absence of either Cyk3 or Hof1 can be suppressed by expression of the hypermorphic allele of the essential chitin synthase II (Chs2), a transmembrane protein transported on secretory vesicles that makes the primary septum during cytokinesis. Spa2 also interacts directly with the chitin synthase Chs2. Interestingly, artificial incorporation of Chs2 into the cytokinetic machinery allows the localisation of Spa2 at the site of division. In addition, increased Spa2 protein levels promote Chs2 incorporation at the site of division and primary septum formation. Our data indicate that Spa2 is recruited to the cleavage site to co-operate with the secretory vesicle system and particular actomyosin ring components to promote the incorporation of Chs2 into the so-called 'ingression progression complexes' during cytokinesis in budding yeast.

摘要

在真核细胞的胞质分裂过程中,额外的质膜和货物的沉积必须与肌动球蛋白环收缩、质膜内陷和细胞外基质重塑相协调。分泌途径促进关键因子特异性掺入胞质分裂机制的过程还知之甚少。在这里,我们表明,细胞极性蛋白 Spa2 在胞质分裂过程中与肌动球蛋白环成分相互作用。Spa2 直接结合胞质分裂因子 Cyk3 和 Hof1。在没有 Cyk3 或 Hof1 的情况下删除 SPA2 基因的致死效应可以通过表达必需的几丁质合酶 II(Chs2)的超突变等位基因来抑制,Chs2 是一种跨膜蛋白,在分泌小泡上运输,在胞质分裂过程中形成主要隔膜。Spa2 还与几丁质合酶 Chs2 直接相互作用。有趣的是,人工将 Chs2 纳入胞质分裂机制可以使 Spa2 定位于分裂部位。此外,增加 Spa2 蛋白水平促进 Chs2 在分裂部位的掺入和初级隔膜的形成。我们的数据表明,Spa2 被招募到切割位点,与分泌小泡系统和特定的肌动球蛋白环成分合作,促进 Chs2 在出芽酵母的胞质分裂过程中被纳入所谓的“内陷进展复合物”。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/300afe05aa2a/pgen.1007299.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/00e95242ea25/pgen.1007299.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/392b66c313f1/pgen.1007299.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/f2e4a9445584/pgen.1007299.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/f4619621758f/pgen.1007299.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/8f08e0aec205/pgen.1007299.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/50efee7a5c91/pgen.1007299.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/24f91c7b43dc/pgen.1007299.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/68ef868b52b1/pgen.1007299.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/b3079040e28d/pgen.1007299.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/300afe05aa2a/pgen.1007299.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/00e95242ea25/pgen.1007299.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/392b66c313f1/pgen.1007299.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/f2e4a9445584/pgen.1007299.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/f4619621758f/pgen.1007299.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/8f08e0aec205/pgen.1007299.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/50efee7a5c91/pgen.1007299.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/24f91c7b43dc/pgen.1007299.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/68ef868b52b1/pgen.1007299.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/b3079040e28d/pgen.1007299.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08c2/5895073/300afe05aa2a/pgen.1007299.g010.jpg

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