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エンドウ トシヤ
ENDO TOSHIYA
遠藤 斗志也 所属 京都産業大学 生命科学部 先端生命科学科 職種 客員教授 |
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| 言語種別 | 英語 |
| 発行・発表の年月 | 2016/08 |
| 形態種別 | 研究論文 |
| 査読 | 査読あり |
| 標題 | Quality control of nonstop membrane proteins at the ER membrane and in the cytosol |
| 執筆形態 | その他 |
| 掲載誌名 | SCIENTIFIC REPORTS |
| 出版社・発行元 | NATURE PUBLISHING GROUP |
| 巻・号・頁 | 6,pp.30795 |
| 著者・共著者 | Shunsuke Arakawa,Kaori Yunoki,Toshiaki Izawa,Yasushi Tamura,Shuh-ichi Nishikawa,Toshiya Endo |
| 概要 | Since messenger RNAs without a stop codon (nonstop mRNAs) for organelle-targeted proteins and their translation products (nonstop proteins) generate clogged translocon channels as well as stalled ribosomes, cells have mechanisms to degrade nonstop mRNAs and nonstop proteins and to clear the translocons (e.g. the Sec61 complex) by release of nonstop proteins into the organellar lumen. Here we followed the fate of nonstop endoplasmic reticulum (ER) membrane proteins with different membrane topologies in yeast to evaluate the importance of the Ltn1-dependent cytosolic degradation and the Dom34-dependent release of the nonstop membrane proteins. Ltn1-dependent degradation differed for membrane proteins with different topologies and its failure did not affect ER protein import or cell growth. On the other hand, failure in the Dom34-dependent release of the nascent polypeptide from the ribosome led to the block of the Sec61 channel and resultant inhibition of other protein import into the ER caused cell growth defects. Therefore, the nascent chain release from the translation apparatus is more instrumental in clearance of the clogged ER translocon channel and thus maintenance of normal cellular functions. |
| DOI | 10.1038/srep30795 |
| ISSN | 2045-2322 |
| PMID | 27481473 |