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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Myosin-X is a molecular motor that functions in filopodia formation
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Myosin-X is a molecular motor that functions in filopodia formation

机译：Myosin-X是一种分子运动，可在丝状伪足形成中起作用

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Despite recent progress in understanding lamellipodia extension, the molecular mechanisms regulating filopodia formation remain largely unknown. Myo10 is a MyTH4-FERM myosin that localizes to the tips of filopodia and is hypothesized to function in filopodia formation. To determine whether endogenous MyolO is required for filopodia formation, we have used scanning EM to assay the numerous filopodia normally present on the dorsal surfaces of HeLa cells. We show here that siRNA-mediated knockdown of Myo1O in HeLa cells leads to a dramatic loss of dorsal filopodia. Overexpressing the coiled coil region from MyolO as a dominantnegative also leads to a loss of dorsal filopodia, thus providing independent evidence that Myo10 functions in filopodia formation. We also show that expressing Myo10 in COS-7 cells, a cell line that normally lacks dorsal filopodia, leads to a massive induction of dorsal filopodia. Because the dorsal filopodia induced by Myo10 are not attached to the substrate, Myo10 can promote filopodia by a mechanism that is independent of substrate attachment. Consistent with this observation, a Myo10 construct that lacks the FERM domain, the region that binds to integrin, retains the ability to induce dorsal filopodia. Deletion of the MyTH4-FERM region, however, completely abolishes Myo10's filopodia-promoting activity, as does deletion of the motor domain. Additional experiments on the mechanism of Myo10 action indicate that it acts downstream of Cdc42 and can promote filopodia in the absence of VASP proteins. Together, these data demonstrate that Myo10 is a molecular motor that functions in filopodia formation.
机译：尽管最近在了解片状脂蛋白的延伸方面取得了进展，但是调节丝状伪足形成的分子机制仍是未知的。 Myo10是一种MyTH4-FERM肌球蛋白，其定位在丝状伪足的尖端，并被认为在丝状伪足形成中起作用。为了确定是否需要内源性MyolO来形成丝状伪足，我们使用扫描电镜来分析通常存在于HeLa细胞背表面的大量丝状伪足。我们在这里显示，在HeLa细胞中siRNA介导的Myo1O的敲低导致背侧丝状伪足的急剧丧失。从MyolO中过度表达卷曲螺旋区域作为显性阴性也导致背侧丝状伪足的丧失，因此提供了Myo10在丝状伪足形成中起作用的独立证据。我们还表明，在COS-7细胞（一种通常缺乏背丝状伪足的细胞系）中表达Myo10会导致对背丝状伪足的大量诱导。由于Myo10诱导的背足丝虫未附着在基质上，因此Myo10可以通过独立于基质附着的机制促进丝状伪足。与该观察结果一致，缺乏FERM结构域（与整联蛋白结合的区域）的Myo10构建体保留了诱导背侧丝状伪足的能力。但是，MyTH4-FERM区域的删除完全消除了Myo10的丝状伪足促进活性，而运动域的删除也没有。关于Myo10作用机理的其他实验表明，它在Cdc42的下游起作用，并且在不存在VASP蛋白的情况下可以促进丝状伪足。这些数据加在一起表明，Myo10是分子运动的，在丝状伪足形成中起作用。

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