MyRIP, a novel Rab effector, enables myosin VIIa recruitment to retinal melanosomes
MyRIP, a novel Rab effector, enables myosin VIIa recruitment to retinal melanosomes
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DOI：
10.1093/embo-reports/kvf090
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发表时间：
2002-05-01
期刊：
影响因子：
7.7
通讯作者：
Petit, C
中科院分区：
文献类型：
--
作者：
El-Amraoui, A;Schonn, JS;Petit, C
肌球蛋白Vila运动蛋白的缺陷会导致人类和小鼠耳聋和视网膜异常。我们报道了一种新的肌球蛋白-V1a相互作用蛋白的鉴定，我们将其命名为MyRIP(Myosin-V11a-and Rab-Interaction Protein)，因为它也以GTP依赖的方式与Rab27A结合。在视网膜色素上皮细胞中，MyRIP、Myosin Vila和Rab27A与黑素小体相关。在转染的PC12细胞中，MyRIP的过表达干扰了肌球蛋白Vila尾部的定位。我们认为，由Rab27A、MyRIP和Myosin Vila组成的分子复合体将视网膜黑素体桥接到肌动蛋白细胞骨架上，从而介导这些细胞器的局部运输。这种分子复合体的缺陷可能解释了在myosinV11a缺陷小鼠的视网膜色素上皮细胞中观察到的黑素小体在核周围的错误定位。
Defects of the myosin Vila motor protein cause deafness and retinal anomalies in humans and mice. We report on the identification of a novel myosin-Vila-interacting protein that we have named MyRIP (myosin-Vlla- and Rab-interacting protein), since it also binds to Rab27A in a GTP-dependent manner. In the retinal pigment epithelium cells, MyRIP, myosin Vila and Rab27A are associated with melanosomes. In transfected PC12 cells, overexpression of MyRIP was shown to interfere with the myosin Vila tail localization. We propose that a molecular complex composed of Rab27A, MyRIP and myosin Vila bridges retinal melanosomes to the actin cytoskeleton and thereby mediates the local trafficking of these organelles. The defect of this molecular complex is likely to account for the perinuclear mislocalization of the melanosomes observed in the retinal pigment epithelium cells of myosinVlla-defective mice.