Rab27A and its effector MyRIP link secretory granules to F-actin and control their motion towards release sites.
Rab27A and its effector MyRIP link secretory granules to F-actin and control their motion towards release sites.
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Rab27a及其效应子myrip将分泌颗粒与F-肌动蛋白联系起来，并控制其向释放位点的运动。
DOI：
10.1083/jcb.200302157
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发表时间：
2003-11-10
影响因子：
7.8
通讯作者：
Darchen, Francois
中科院分区：
文献类型：
--
作者：
Desnos, Claire;Schonn, Jean-Sebastien;Huet, Sebastien;Tran, Viet Samuel;El-Amraoui, Aziz;Raposo, Graca;Fanget, Isabelle;Chapuis, Catherine;Menasche, Gael;de Saint Basile, Genevieve;Petit, Christine;Cribier, Sophie;Henry, Jean-Pierre;Darchen, Francois
GTribRab 27 A通过MyRIP或亲黑素蛋白与肌球蛋白-VIIa和肌球蛋白-Va相互作用，并介导黑素体与肌动蛋白的结合。在这里，我们发现Rab 27 A和MyRIP与肾上腺嗜铬细胞和PC 12细胞中的分泌颗粒（SGs）相关。Rab 27 A、GTP酶缺陷型Rab 27 A-Q78 L或MyRIP的过表达降低了PC 12细胞的分泌反应。单个肾上腺嗜铬细胞的电流记录显示Rab 27 A-Q78 L和MyRIP减少了持续释放的成分。此外，这些对分泌的影响被肌动蛋白解聚药物latrunculin部分抑制，但被jasplakinastatin稳定肌动蛋白皮质加强。最后，MyRIP和Rab 27 A-Q78 L限制了PC 12细胞质膜下区域中SGs的运动，如通过渐逝波荧光显微镜所测量的。与此相反，Rab 27 A结合域的MyRIP和MyRIP结构，与肌球蛋白-Va，但不与肌动蛋白的相互作用增加的流动性的SG。我们建议Rab 27 A和MyRIP连接SGs的F-肌动蛋白和控制他们的运动通过肌动蛋白皮质释放网站。
The GTPase Rab27A interacts with myosin-VIIa and myosin-Va via MyRIP or melanophilin and mediates melanosome binding to actin. Here we show that Rab27A and MyRIP are associated with secretory granules (SGs) in adrenal chromaffin cells and PC12 cells. Overexpression of Rab27A, GTPase-deficient Rab27A-Q78L, or MyRIP reduced secretory responses of PC12 cells. Amperometric recordings of single adrenal chromaffin cells revealed that Rab27A-Q78L and MyRIP reduced the sustained component of release. Moreover, these effects on secretion were partly suppressed by the actin-depolymerizing drug latrunculin but strengthened by jasplakinolide, which stabilizes the actin cortex. Finally, MyRIP and Rab27A-Q78L restricted the motion of SGs in the subplasmalemmal region of PC12 cells, as measured by evanescent-wave fluorescence microscopy. In contrast, the Rab27A-binding domain of MyRIP and a MyRIP construct that interacts with myosin-Va but not with actin increased the mobility of SGs. We propose that Rab27A and MyRIP link SGs to F-actin and control their motion toward release sites through the actin cortex.