Steele F, O'Tousa J E
Department of Biological Sciences, University of Notre Dame, Indiana 46556.
Neuron. 1990 Jun;4(6):883-90. doi: 10.1016/0896-6273(90)90141-2.
Drosophila rdgC (retinal degeneration-C) mutants show normal retinal morphology and photoreceptor physiology at young ages. Dark-reared rdgC flies retain this wild-type phenotype, but light-reared mutants undergo retinal degeneration. rdgC photoreceptors with low levels of rhodopsin as a result of vitamin A deprivation or a mutant rhodopsin (ninaE) gene fail to show rdgC-induced degeneration even after prolonged light treatment, demonstrating that degeneration occurs as a result of light stimulation of rhodopsin. Analysis of norpA; rdgC flies shows that the norpA-encoded phospholipase C, the target enzyme of the G protein activated by rhodopsin, is not required for rdgC-induced degeneration. Thus the rdgC+ gene product is required to prevent retinal degeneration that results from a previously unrecognized consequence of rhodopsin stimulation.
果蝇rdgC(视网膜变性-C)突变体在幼年时视网膜形态和光感受器生理功能正常。黑暗饲养的rdgC果蝇保持这种野生型表型,但光照饲养的突变体则会发生视网膜变性。由于维生素A缺乏或突变的视紫红质(ninaE)基因导致视紫红质水平较低的rdgC光感受器,即使经过长时间光照处理也不会出现rdgC诱导的变性,这表明变性是视紫红质光刺激的结果。对norpA; rdgC果蝇的分析表明,norpA编码的磷脂酶C(视紫红质激活的G蛋白的靶酶)对于rdgC诱导的变性不是必需的。因此,rdgC+基因产物是预防视网膜变性所必需的,而这种变性是由视紫红质刺激先前未被认识到的后果导致的。