Disease relevance of rdgC

• Mutations in rdgC result in defects in termination of the light response and cause severe retinal degeneration [1].

High impact information on rdgC

• Molecular analysis shows that the rdgC transcription unit encodes a novel serine/threonine protein phosphatase [2].
• The Drosophila retinal degeneration C (rdgC) gene is required to prevent light-induced retinal degeneration [2].
• Drosophila retinal degeneration C (rdgC) encodes a novel serine/threonine protein phosphatase [2].
• We found that retinal cell death in rdgC and ninaE(RH27)/+ flies occurred by apoptosis and was blocked by eye-specific expression of the baculoviral cell survival protein p35 [3].
• Drosophila RDGC (retinal degeneration C) is a phosphatase required for rhodopsin dephosphorylation in vivo [4].

Chemical compound and disease context of rdgC

• Through our transcriptional mapping effort in the Xp22 region, we have isolated by exon trapping a new transcript highly homologous to the Drosophila retinal degeneration C (rdgC) gene. rdgC encodes a serine/threonine phosphatase protein and is required in Drosophila to prevent light-induced retinal degeneration [5].

Biological context of rdgC

• The Drosophila retinal degeneration C (rdgC) gene encodes an unusual protein serine/threonine phosphatase in that it contains at least two EF-hand motifs at its carboxy terminus [6].

Anatomical context of rdgC

• Drosophila rdgC (retinal degeneration-C) mutants show normal retinal morphology and photoreceptor physiology at young ages [7].
• While rdgC is expressed in the visual system of the fly, as well as in the mushroom bodies of the central brain, we found that Ppef is highly expressed in sensory neurons of the dorsal root ganglia (DRG) and neural crest-derived cranial ganglia [5].
• A novel human serine-threonine phosphatase related to the Drosophila retinal degeneration C (rdgC) gene is selectively expressed in sensory neurons of neural crest origin [5].

Other interactions of rdgC

• In contrast, no decrease was observed in the amounts of Rh1 metarhodopsin recovered from illuminated flies which were deficient either in the eye-specific phosphatase (rdgC mutant) or in the eye-specific phospholipase C (norpA(H24) and norpA(H52) mutants) [8].

References