ArticlePloS one2011
Specific interaction of Gαi3 with the Oa1 G-protein coupled receptor controls the size and density of melanosomes in retinal pigment epithelium.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
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- Conversations with Ray Guillery on albinism: linking Siamese cat visual pathway connectivity to mouse retinal development.The European journal of neuroscience · 2019Review
- Ocular Albinism Type 1 Regulates Deltamethrin Tolerance inFrontiers in physiology · 2019Article
- RNA-binding protein Rbpms is represented in human retinas by isoforms A and C and its transcriptional regulation involves Sp1-binding site.Molecular genetics and genomics : MGG · 2018Article
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- GPR143 Gene Mutations in Five Chinese Families with X-linked Congenital Nystagmus.Scientific reports · 2015Article
- Location-dependent signaling of the group 1 metabotropic glutamate receptor mGlu5.Molecular pharmacology · 2014Review
- A constitutively active Gαi3 protein corrects the abnormal retinal pigment epithelium phenotype of Oa1-/- mice.PloS one · 2013Article
- Melanoregulin, product of the dsu locus, links the BLOC-pathway and OA1 in organelle biogenesis.PloS one · 2012Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundOcular albinism type 1, an X-linked disease characterized by the presence of enlarged melanosomes in the retinal pigment epithelium (RPE) and abnormal crossing of axons at the optic chiasm, is caused by mutations in the OA1 gene. The protein product of this gene is a G-protein-coupled receptor (GPCR) localized in RPE melanosomes. The Oa1-/- mouse model of ocular albinism reproduces the human disease. Oa1 has been shown to immunoprecipitate with the Gαi subunit of heterotrimeric G proteins from human skin melanocytes. However, the Gαi subfamily has three highly homologous members, Gαi1, Gαi2 and Gαi3 and it is possible that one or more of them partners with Oa1. We had previously shown by in-vivo studies that Gαi3-/- and Oa1-/- mice have similar RPE phenotype and decussation patterns. In this paper we analyze the specificity of the Oa1-Gαi interaction. METHODOLOGY: By using the genetic mouse models Gαi1-/-, Gαi2-/-, Gαi3-/- and the double knockout Gαi1-/-, Gαi3-/- that lack functional Gαi1, Gαi2, Gαi3, or both Gαi1 and Gαi3 proteins, respectively, we show that Gαi3 is critical for the maintenance of a normal melanosomal phenotype and that its absence is associated with changes in melanosomal size and density. GST-pull-down and immunoprecipitation assays conclusively demonstrate that Gαi3 is the only Gαi that binds to Oa1. Western blots show that Gαi3 expression is barely detectable in the Oa1-/- RPE, strongly supporting a previously unsuspected role for Gαi3 in melanosomal biogenesis.
conclusionOur results identify the Oa1 transducer Gαi3 as the first downstream component in the Oa1 signaling pathway.
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