Rescue of photoreceptor degeneration in rhodopsin-null Drosophila mutants by activated Rac1
Rescue of photoreceptor degeneration in rhodopsin-null Drosophila mutants by activated Rac1
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DOI：
10.1126/science.290.5498.1978
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发表时间：
2000-12-08
期刊：
影响因子：
56.9
通讯作者：
Ready, DF
中科院分区：
文献类型：
--
作者：
Chang, HY;Ready, DF
视紫红质是光感受器形态发生所必需的；缺乏视紫红质的光感受器在人类、小鼠和果蝇中退化。在这里，我们报道了转基因表达显性活性的果蝇Rho鸟苷三磷酸酶Drac1挽救了视紫红质缺失突变体的光感受器形态发生；显性负性Drac1的表达导致了与视紫红质缺失突变体中看到的表型相似的表型。DRA1定位于光感受器皮质肌动蛋白细胞骨架的专门化，在视紫红质缺失突变体中缺失。因此，视紫红质似乎通过DRA1来组织肌动蛋白细胞骨架，贡献了一种结构支持--这对光感受器的形态发生至关重要。
Rhodopsin is essential for photoreceptor morphogenesis; photoreceptors lacking rhodopsin degenerate in humans, mice, and Drosophila. Here we report that transgenic expression of a dominant-active Drosophila Rho guanosine triphosphatase, Drac1, rescued photoreceptor morphogenesis in rhodopsin-null mutants; expression of dominant-negative Drac1 resulted in a phenotype similar to that seen in rhodopsin-null mutants. Drac1 was localized in a specialization of the photoreceptor cortical actin cytoskeleton, which was lost in rhodopsin-null mutants. Thus, rhodopsin appears to organize the actin cytoskeleton through Drac1, contributing a structural support-essential for photoreceptor morphogenesis.