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首页> 外文期刊>Molecular and Cellular Biology >A Drosophila homolog of the Rac- and Cdc42-activated serine/threonine kinase PAK is a potential focal adhesion and focal complex protein that colocalizes with dynamic actin structures.
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A Drosophila homolog of the Rac- and Cdc42-activated serine/threonine kinase PAK is a potential focal adhesion and focal complex protein that colocalizes with dynamic actin structures.

机译：Rac和Cdc42激活的丝氨酸/苏氨酸激酶PAK的果蝇同源物是与动态肌动蛋白结构共定位的潜在粘着斑和病灶复合蛋白。

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Changes in cell morphology are essential in the development of a multicellular organism. The regulation of the cytoskeleton by the Rho subfamily of small GTP-binding proteins is an important determinant of cell shape. The Rho subfamily has been shown to participate in a variety of morphogenetic processes during Drosophila melanogaster development. We describe here a Drosophila homolog, DPAK, of the serine/threonine kinase PAK, a protein which is a target of the Rho subfamily proteins Rac and Cdc42. Rac, Cdc42, and PAK have previously been implicated in signaling by c-Jun amino-terminal kinases. DPAK bound to activated (GTP-bound) Drosophila Rac (DRacA) and Drosophila Cdc42. Similarities in the distributions of DPAK, integrin, and phosphotyrosine suggested an association of DPAK with focal adhesions and Cdc42- and Rac-induced focal adhesion-like focal complexes. DPAK was elevated in the leading edge of epidermal cells, whose morphological changes drive dorsal closure of the embryo. We have previously shown that the accumulation of cytoskeletal elements initiating cell shape changes in these cells could be inhibited by expression of a dominant-negative DRacA transgene. We show that leading-edge epidermal cells flanking segment borders, which express particularly large amounts of DPAK, undergo transient losses of cytoskeletal structures during dorsal closure. We propose that DPAK may be regulating the cytoskeleton through its association with focal adhesions and focal complexes and may be participating with DRacA in a c-Jun amino-terminal kinase signaling pathway recently demonstrated to be required for dorsal closure.
机译：细胞形态的变化对于多细胞生物的发育至关重要。小GTP结合蛋白的Rho亚家族对细胞骨架的调节是细胞形状的重要决定因素。 Rho亚科已被证明在果蝇的发育过程中参与了多种形态发生过程。我们在此描述果蝇/苏氨酸激酶PAK的果蝇同源物DPAK，该蛋白是Rho亚家族蛋白Rac和Cdc42的靶标。 Rac，Cdc42和PAK之前已涉及c-Jun氨基末端激酶的信号传导。 DPAK绑定到激活的（GTP绑定）果蝇Rac（DRacA）和果蝇Cdc42。 DPAK，整联蛋白和磷酸酪氨酸分布的相似性表明DPAK与粘着斑以及Cdc42和Rac诱导的粘着斑样粘着复合物相关。 DPAK在表皮细胞的前缘升高，其形态变化驱动胚胎的背侧闭合。先前我们已经表明，通过显性阴性DRacA转基因的表达可以抑制这些细胞中启动细胞形状变化的细胞骨架元素的积累。我们显示，前沿的表皮细胞侧翼段边界，其表达特别大量的DPAK，在背侧闭合期间经历细胞骨架结构的瞬时损失。我们建议DPAK可能通过其与粘着斑和病灶复合物的关联来调节细胞骨架，并且可能与DRacA参与最近被证明需要闭合背的c-Jun氨基末端激酶信号通路。

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