Drosophila fabp is required for light-dependent Rhodopsin-1 clearance and photoreceptor survival.

Rhodopsins are light-detecting proteins coupled with retinal chromophores essential for visual function. Coincidentally, dysfunctional Rhodopsin homeostasis underlies retinal degeneration in humans and model organisms. Drosophila ninaEG69D mutant is one such example, where the encoded Rh1 protein im...

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Autores principales:	Huai-Wei Huang, Hyung Don Ryoo
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Genetics QH426-470
Acceso en línea:	https://doaj.org/article/9bc2897276d94de69b067c2936c5bc22
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spelling	oai:doaj.org-article:9bc2897276d94de69b067c2936c5bc222021-12-02T20:03:28ZDrosophila fabp is required for light-dependent Rhodopsin-1 clearance and photoreceptor survival.1553-73901553-740410.1371/journal.pgen.1009551https://doaj.org/article/9bc2897276d94de69b067c2936c5bc222021-10-01T00:00:00Zhttps://doi.org/10.1371/journal.pgen.1009551https://doaj.org/toc/1553-7390https://doaj.org/toc/1553-7404Rhodopsins are light-detecting proteins coupled with retinal chromophores essential for visual function. Coincidentally, dysfunctional Rhodopsin homeostasis underlies retinal degeneration in humans and model organisms. Drosophila ninaEG69D mutant is one such example, where the encoded Rh1 protein imposes endoplasmic reticulum (ER) stress and causes light-dependent retinal degeneration. The underlying reason for such light-dependency remains unknown. Here, we report that Drosophila fatty acid binding protein (fabp) is a gene induced in ninaEG69D/+ photoreceptors, and regulates light-dependent Rhodopsin-1 (Rh1) protein clearance and photoreceptor survival. Specifically, our photoreceptor-specific gene expression profiling study in ninaEG69D/+ flies revealed increased expression of fabp together with other genes that control light-dependent Rh1 protein degradation. fabp induction in ninaEG69D photoreceptors required vitamin A and its transporter genes. In flies reared under light, loss of fabp caused an accumulation of Rh1 proteins in cytoplasmic vesicles. The increase in Rh1 levels under these conditions was dependent on Arrestin2 that mediates feedback inhibition of light-activated Rh1. fabp mutants exhibited light-dependent retinal degeneration, a phenotype also found in other mutants that block light-induced Rh1 degradation. These observations reveal a previously unrecognized link between light-dependent Rh1 proteostasis and the ER-stress imposing ninaEG69D mutant that cause retinal degeneration.Huai-Wei HuangHyung Don RyooPublic Library of Science (PLoS)articleGeneticsQH426-470ENPLoS Genetics, Vol 17, Iss 10, p e1009551 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Genetics QH426-470
spellingShingle	Genetics QH426-470 Huai-Wei Huang Hyung Don Ryoo Drosophila fabp is required for light-dependent Rhodopsin-1 clearance and photoreceptor survival.
description	Rhodopsins are light-detecting proteins coupled with retinal chromophores essential for visual function. Coincidentally, dysfunctional Rhodopsin homeostasis underlies retinal degeneration in humans and model organisms. Drosophila ninaEG69D mutant is one such example, where the encoded Rh1 protein imposes endoplasmic reticulum (ER) stress and causes light-dependent retinal degeneration. The underlying reason for such light-dependency remains unknown. Here, we report that Drosophila fatty acid binding protein (fabp) is a gene induced in ninaEG69D/+ photoreceptors, and regulates light-dependent Rhodopsin-1 (Rh1) protein clearance and photoreceptor survival. Specifically, our photoreceptor-specific gene expression profiling study in ninaEG69D/+ flies revealed increased expression of fabp together with other genes that control light-dependent Rh1 protein degradation. fabp induction in ninaEG69D photoreceptors required vitamin A and its transporter genes. In flies reared under light, loss of fabp caused an accumulation of Rh1 proteins in cytoplasmic vesicles. The increase in Rh1 levels under these conditions was dependent on Arrestin2 that mediates feedback inhibition of light-activated Rh1. fabp mutants exhibited light-dependent retinal degeneration, a phenotype also found in other mutants that block light-induced Rh1 degradation. These observations reveal a previously unrecognized link between light-dependent Rh1 proteostasis and the ER-stress imposing ninaEG69D mutant that cause retinal degeneration.
format	article
author	Huai-Wei Huang Hyung Don Ryoo
author_facet	Huai-Wei Huang Hyung Don Ryoo
author_sort	Huai-Wei Huang
title	Drosophila fabp is required for light-dependent Rhodopsin-1 clearance and photoreceptor survival.
title_short	Drosophila fabp is required for light-dependent Rhodopsin-1 clearance and photoreceptor survival.
title_full	Drosophila fabp is required for light-dependent Rhodopsin-1 clearance and photoreceptor survival.
title_fullStr	Drosophila fabp is required for light-dependent Rhodopsin-1 clearance and photoreceptor survival.
title_full_unstemmed	Drosophila fabp is required for light-dependent Rhodopsin-1 clearance and photoreceptor survival.
title_sort	drosophila fabp is required for light-dependent rhodopsin-1 clearance and photoreceptor survival.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/9bc2897276d94de69b067c2936c5bc22
work_keys_str_mv	AT huaiweihuang drosophilafabpisrequiredforlightdependentrhodopsin1clearanceandphotoreceptorsurvival AT hyungdonryoo drosophilafabpisrequiredforlightdependentrhodopsin1clearanceandphotoreceptorsurvival
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Drosophila fabp is required for light-dependent Rhodopsin-1 clearance and photoreceptor survival.

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