Abelson kinase (Abl) and RhoGEF2 regulate actin organization during cell constriction in Drosophila
Abelson kinase (Abl) and RhoGEF2 regulate actin organization during cell constriction in Drosophila
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DOI：
10.1242/dev.02748
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发表时间：
2007-02-01
期刊：
影响因子：
4.6
通讯作者：
Peifer, Mark
中科院分区：
文献类型：
--
作者：
Fox, Donald T.;Peifer, Mark
形态发生涉及不同细胞骨架调节因子的相互作用。研究它们在特定的形态发生事件中是如何相互作用的，将有助于我们了解动物的发育。腹侧沟的形成是果蝇原肠发育过程中的一种形态发生事件，研究已经确定了一条涉及G蛋白凝集素(CTA)和Rho激活剂RhoGEF2的信号通路。尽管这些调节因子促进稳定的肌球蛋白积累和顶端细胞收缩，但这些通路成员的功能丧失表型并不相同，这表明存在额外的腹沟调节因子。在这里，我们报告了Abelson激酶(Abl)作为一种新的腹沟调节因子的鉴定。我们发现，在腹侧沟形成过程中，Abl在顶端起作用，抑制中胚层细胞中EnA和肌动蛋白的积累。此外，RhoGEF2还调节腹沟形成过程中有序的肌动蛋白定位，而其激活剂CTA则不调节。综上所述，我们的数据表明，腹侧沟顶端收缩有两个关键的先决条件：由CTA和RhoGEF2调节的肌球蛋白稳定/激活；以及由Ab1和RhoGEF2调节的顶端肌动蛋白的组织。这些观察确定了Abl的一个重要的形态发生作用，并暗示了该激酶在顶端细胞收缩过程中的一种保守机制。
Morphogenesis involves the interplay of different cytoskeletal regulators. Investigating how they interact during a given morphogenetic event will help us understand animal development. Studies of ventral furrow formation, a morphogenetic event during Drosophila gastrulation, have identified a signaling pathway involving the G-protein Concertina (Cta) and the Rho activator RhoGEF2. Although these regulators act to promote stable myosin accumulation and apical cell constriction, loss-of-function phenotypes for each of these pathway members is not equivalent, suggesting the existence of additional ventral furrow regulators. Here, we report the identification of Abelson kinase (Abl) as a novel ventral furrow regulator. We find that Abl acts apically to suppress the accumulation of both Enabled (Ena) and actin in mesodermal cells during ventral furrow formation. Further, RhoGEF2 also regulates ordered actin localization during ventral furrow formation, whereas its activator, Cta, does not. Taken together, our data suggest that there are two crucial preconditions for apical constriction in the ventral furrow: myosin stabilization/activation, regulated by Cta and RhoGEF2; and the organization of apical actin, regulated by Abl and RhoGEF2. These observations identify an important morphogenetic role for Abl and suggest a conserved mechanism for this kinase during apical cell constriction.