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首页> 外文期刊>Current Biology: CB >A role for kinesin-2 in COPI-dependent recycling between the ER and the golgi complex
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A role for kinesin-2 in COPI-dependent recycling between the ER and the golgi complex

机译：驱动蛋白2在ER和高尔基体之间的COPI依赖性循环中的作用

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Transport carriers operating between early compartments in the mammalian secretory pathway have to travel long distances in the cell by mostly relying on the microtubule network and its associated motor proteins. Although anterograde transport from the endoplasmic reticulum (ER) to the Golgi complex is mediated by cytoplasmic dynein [1, 2], the identity of the motor(s) mediating transport in the retrograde direction is presently unclear. Some studies have suggested that the heterotrimeric kinesin-2 complex plays a role in transport between the ER and the Golgi [3, 4]. Here, we have examined kinesin-2 function by using an RNA-interference approach to downregulate the expression of KAP3, the nonmotor subunit of kinesin-2, in HeLa cells. KAP3 silencing results in the fragmentation of the Golgi apparatus and a change in the steady-state localization of the KDEL-receptor (KDEL-R). Using specific transport assays, we show that the rate of anterograde secretory traffic is unaffected in these cells but that KDEL-R-dependent retrograde transport is strongly abrogated. Our data strongly support a role for kinesin-2 in the KDEL-R-/COPI-dependent retrograde transport pathway from the Golgi complex to the ER.
机译：在哺乳动物分泌途径的早期区室之间运行的转运载体必须主要依靠微管网络及其相关的运动蛋白在细胞中长距离传播。尽管从内质网（ER）到高尔基复合体的顺行转运是由细胞质动力蛋白介导的[1，2]，但目前尚不清楚介导逆行方向转运的马达的身份。一些研究表明，异源三聚体驱动蛋白2复合物在ER和高尔基体之间的转运中发挥作用[3，4]。在这里，我们已经通过使用RNA干扰方法来下调kinesin-2的功能，从而下调HeLa细胞中kinesin-2的非运动亚基KAP3的表达。 KAP3沉默导致高尔基体碎裂和KDEL受体（KDEL-R）的稳态定位发生变化。使用特定的运输测定，我们表明顺行性分泌运输的速率在这些细胞中不受影响，但KDEL-R依赖的逆行运输被强烈废除。我们的数据强烈支持驱动蛋白2在从高尔基复合体到ER的KDEL-R- / COPI依赖性逆行转运途径中的作用。

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