Rer1p regulates the ER retention of immature rhodopsin and modulates its intracellular trafficking

Ken Sato, Akinori Yamasaki, Taichi Hara, Ikuko Maejima, Miyuki Sato, Katsuya Sato

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Rhodopsin is a pigment in photoreceptor cells. Some rhodopsin mutations cause the protein to accumulate in the endoplasmic reticulum (ER), leading to photoreceptor degeneration. Although several mutations have been reported, how mutant rhodopsin is retained in the ER remains unclear. In this study, we identified Rer1p as a modulator of ER retention and rhodopsin trafficking. Loss of Rer1p increased the transport of wild-type rhodopsin to post-Golgi compartments. Overexpression of Rer1p caused immature wild-type rhodopsin to accumulate in the ER. Interestingly, the G51R rhodopsin mutant, which has a mutation in the first transmembrane domain and accumulates in the ER, was released to the plasma membrane or lysosomes in Rer1-knockdown cells. Consistent with these results, Rer1p interacted with both wild-type and mutant rhodopsin. These results suggest that Rer1p regulates the ER retention of immature or misfolded rhodopsin and modulates its intracellular trafficking through the early secretory pathway.

Original languageEnglish
Article number5973
JournalScientific reports
Volume4
DOIs
Publication statusPublished - 2014 Aug 6

ASJC Scopus subject areas

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