MYO1C stabilizes actin and facilitates the arrival of transport carriers at the Golgi complex
MYO1C stabilizes actin and facilitates the arrival of transport carriers at the Golgi complex
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DOI：
10.1242/jcs.225029
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发表时间：
2019-04-01
影响因子：
4
通讯作者：
Schauer, Kristine
中科院分区：
文献类型：
--
作者：
Capmany, Anahi;Yoshimura, Azumi;Schauer, Kristine
在这项研究中，我们的目的是鉴定控制高尔基复合体运输的肌球蛋白运动蛋白。除了已知的高尔基体相关肌球蛋白 MYO6、MYO18A 和 MYH9（肌球蛋白 IIA）之外，我们还发现 MYO1C 是人类细胞系中高尔基体的新参与者。我们证明 MYO1C 的耗竭会诱导高尔基复合体断裂和解压缩。 MYO1C 在高尔基复合体周围的动态结构中积累，与高尔基相关肌动蛋白点共定位。 MYO1C 耗竭会导致细胞 F-肌动蛋白丢失，并且在抑制或丢失肌动蛋白相关蛋白 2/3 复合物 Arp2/3（也称为 ARPC）后也会观察到高尔基复合体解压。我们表明，MYO1C 耗竭的功能性后果是来自顺行和逆行路线的传入运输载体的到达延迟。我们建议 MYO1C 稳定高尔基复合体的肌动蛋白，促进传入的运输载体到达高尔基体。本文有与该论文第一作者的相关第一人称采访。
In this study, we aimed to identify the myosin motor proteins that control trafficking at the Golgi complex. In addition to the known Golgi-associated myosins MYO6, MYO18A and MYH9 (myosin IIA), we identified MYO1C as a novel player at the Golgi in a human cell line. We demonstrate that depletion of MYO1C induces Golgi complex fragmentation and decompaction. MYO1C accumulates at dynamic structures around the Golgi complex that colocalize with Golgi-associated actin dots. MYO1C depletion leads to loss of cellular F-actin, and Golgi complex decompaction is also observed after inhibition or loss of the actin-related protein 2/3 complex, Arp2/3 (also known as ARPC). We show that the functional consequence of MYO1C depletion is a delay in the arrival of incoming transport carriers, both from the anterograde and retrograde routes. We propose that MYO1C stabilizes actin at the Golgi complex, facilitating the arrival of incoming transport carriers at the Golgi.This article has an associated First Person interview with the first author of the paper.