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Chs7p是一种参与内质网蛋白质输出控制的新蛋白质,它专门参与酿酒酵母中几丁质合成的调控。

Chs7p, a new protein involved in the control of protein export from the endoplasmic reticulum that is specifically engaged in the regulation of chitin synthesis in Saccharomyces cerevisiae.

作者信息

Trilla J A, Durán A, Roncero C

机构信息

Instituto de Microbiología Bioquímica, Consejo Superior de Investigaciones Científicas/Universidad de Salamanca and Departamento de Microbiología y Genética, Universidad de Salamanca 37007 Salamanca, Spain.

出版信息

J Cell Biol. 1999 Jun 14;145(6):1153-63. doi: 10.1083/jcb.145.6.1153.

Abstract

The Saccharomyces cerevisiae CHS7 gene encodes an integral membrane protein located in the ER which is directly involved in chitin synthesis through the regulation of chitin synthase III (CSIII) activity. In the absence of CHS7 product, Chs3p, but not other secreted proteins, is retained in the ER, leading to a severe defect in CSIII activity and consequently, to a reduced rate of chitin synthesis. In addition, chs7 null mutants show the yeast phenotypes associated with a lack of chitin: reduced mating efficiency and lack of the chitosan ascospore layer, clear indications of Chs7p function throughout the S. cerevisiae biological cycle. CHS3 overexpression does not lead to increased levels of CSIII because the Chs3p excess is retained in the ER. However, joint overexpression of CHS3 and CHS7 increases the export of Chs3p from the ER and this is accompanied by a concomitant increase in CSIII activity, indicating that the amount of Chs7p is a limiting factor for CSIII activity. Accordingly, CHS7 transcription is increased when elevated amounts of chitin synthesis are detected. These results show that Chs7p forms part of a new mechanism specifically involved in Chs3p export from the ER and consequently, in the regulation of CSIII activity.

摘要

酿酒酵母CHS7基因编码一种位于内质网的整合膜蛋白,该蛋白通过调节几丁质合酶III(CSIII)的活性直接参与几丁质合成。在没有CHS7产物的情况下,Chs3p而非其他分泌蛋白会滞留在内质网中,导致CSIII活性严重缺陷,进而几丁质合成速率降低。此外,chs7基因缺失突变体表现出与几丁质缺乏相关的酵母表型:交配效率降低以及缺乏壳聚糖子囊孢子层,这清楚地表明Chs7p在酿酒酵母整个生物周期中发挥功能。CHS3的过表达不会导致CSIII水平升高,因为过量的Chs3p会滞留在内质网中。然而,CHS3和CHS7的联合过表达增加了Chs3p从内质网的输出,同时伴随着CSIII活性的相应增加,这表明Chs7p的量是CSIII活性的限制因素。因此,当检测到几丁质合成量增加时,CHS7的转录会增加。这些结果表明,Chs7p构成了一种新机制的一部分,该机制专门参与Chs3p从内质网的输出,从而参与CSIII活性的调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b779/2133151/4ba1946a80bd/JCB9812082.f1.jpg

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