Myosin X is a downstream effector of PI(3)K during phagocytosis
Myosin X is a downstream effector of PI(3)K during phagocytosis
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DOI：
10.1038/ncb805
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发表时间：
2002-07-01
影响因子：
21.3
通讯作者：
Greenberg, S
中科院分区：
文献类型：
--
作者：
Cox, D;Berg, JS;Greenberg, S
吞噬作用是巨噬细胞中磷脂酰肌醇-3-OH-激酶 (PI(3)K) 依赖性过程。我们确定了 Myo10 (Myosin-X)，一种具有普莱克斯特林同源 (PH) 结构域的非常规肌球蛋白，作为 PI(3) K 的潜在下游靶标。Myo10 以渥曼青霉素敏感的方式被招募到吞噬杯中。在巨噬细胞系中表达 Myo10 截短构建体（Myo10 尾部）或在牛肺泡巨噬细胞中负载抗 Myo10 抗体可抑制吞噬作用。相比之下，在其 PH 结构域之一含有点突变的 Myo10 尾部构建体的表达未能抑制吞噬作用。 Myo10 尾部的表达抑制了 IgG 包被基质上的铺展，但不抑制粘附，这与 Myo10 在伪足延伸中的功能一致。我们认为 Myo10 在吞噬作用过程中提供了 PI(3) K 和伪足延伸之间的分子联系。
Phagocytosis is a phosphatidylinositol-3-OH-kinase (PI(3)K)-dependent process in macrophages. We identified Myo10 (Myosin-X), an unconventional myosin with pleckstrin homology (PH) domains, as a potential downstream target of PI(3) K. Myo10 was recruited to phagocytic cups in a wortmannin-sensitive manner. Expression of a truncation construct of Myo10 (Myo10 tail) in a macrophage cell line or cytosolic loading of anti-Myo10 antibodies in bovine alveolar macrophages inhibited phagocytosis. In contrast, expression of a Myo10 tail construct containing a point mutation in one of its PH domains failed to inhibit phagocytosis. Expression of Myo10 tail inhibited spreading, but not adhesion, on IgG-coated substrates, consistent with a function for Myo10 in pseudopod extension. We propose that Myo10 provides a molecular link between PI(3) K and pseudopod extension during phagocytosis.