Loss of the phospholipase C gene product induces massive endocytosis of rhodopsin and arrestin in Drosophila photoreceptors.
Loss of the phospholipase C gene product induces massive endocytosis of rhodopsin and arrestin in Drosophila photoreceptors.
复制标题
磷脂酶 C 基因产物的缺失会诱导果蝇感光体中视紫质和视紫红质的大量内吞作用。
DOI：
10.1016/s0042-6989(01)00229-2
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发表时间：
2002
期刊：
影响因子：
1.8
通讯作者：
Dolph,PatrickJ
中科院分区：
文献类型：
--
作者：
Orem,NicholasR;Dolph,PatrickJ
之前我们已经证明，果蝇中的视觉转导突变体的子集诱导视紫质和视紫红质之间形成稳定的复合物。其中一种突变体存在于视觉系统特异性磷脂酶 C (PLC) 中。 PLC突变体中产生的视紫红质/抑制蛋白复合物会引起大规模的视网膜变性。在这里，我们证明视紫红质和视紫红质在 PLC 突变体背景下都会经历光依赖性内吞作用。有趣的是，内化的视紫红质迅速降解，但抑制蛋白完全稳定。讨论了关于抑制蛋白介导的内吞作用和人类视网膜疾病的机制的数据。
Previously we have shown that a subset of visual transduction mutants in Drosophila melanogaster induce the formation of stable complexes between rhodopsin and arrestin. One such mutant is in a visual system-specific phospholipase C (PLC). The rhodopsin/arrestin complexes generated in PLC mutants induce massive retinal degeneration. Here we demonstrate that both arrestin and rhodopsin undergo light-dependent endocytosis in a PLC mutant background. Interestingly, the internalized rhodopsin is rapidly degraded, but the arrestin is fully stable. The data are discussed with respect to mechanisms of arrestin-mediated endocytosis and human retinal disease.