dPob/EMC is essential for biosynthesis of rhodopsin and other multi-pass membrane proteins in Drosophila photoreceptors
文献类型： 外文期刊
作者： Satoh, Takunori 1 ; Ohba, Aya 1 ; Liu, Ziguang 2 ; Inagaki, Tsuyoshi 1 ; Satoh, Akiko K. 1 ;
作者机构： 1.Hiroshima Univ, Grad Sch Integrated Arts & Sci, Higashihiroshima, Japan
2.Heilongjiang Acad Agr Sci, Inst Anim Husb, Harbin, Peoples R China
期刊名称：ELIFE （ 影响因子：8.14； 五年影响因子：9.056 ）
ISSN： 2050-084X
年卷期： 2015 年 4 卷
页码：
收录情况： SCI
摘要： In eukaryotes, most integral membrane proteins are synthesized, integrated into the membrane, and folded properly in the endoplasmic reticulum (ER). We screened the mutants affecting rhabdomeric expression of rhodopsin 1 (Rh1) in the Drosophila photoreceptors and found that dPob/EMC3, EMC1, and EMC8/9, Drosophila homologs of subunits of ER membrane protein complex (EMC), are essential for stabilization of immature Rh1 in an earlier step than that at which another Rh1-specific chaperone (NinaA) acts. dPob/EMC3 localizes to the ER and associates with EMC1 and calnexin. Moreover, EMC is required for the stable expression of other multi-pass transmembrane proteins such as minor rhodopsins Rh3 and Rh4, transient receptor potential, and Na+K+-ATPase, but not for a secreted protein or type I single-pass transmembrane proteins. Furthermore, we found that dPob/EMC3 deficiency induces rhabdomere degeneration in a light-independent manner. These results collectively indicate that EMC is a key factor in the biogenesis of multi-pass transmembrane proteins, including Rh1, and its loss causes retinal degeneration.
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