Abp1 utilizes the Arp2/3 complex activator Scar/WAVE in bristle development
Abp1 utilizes the Arp2/3 complex activator Scar/WAVE in bristle development
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DOI：
10.1242/jcs.101451
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发表时间：
2012-08-01
影响因子：
4
通讯作者：
Kessels, Michael M.
中科院分区：
文献类型：
--
作者：
Koch, Nicole;Dharmalingam, Elavarasi;Kessels, Michael M.
许多发育过程依赖于皮层肌动蛋白动力学，然而，其在细胞皮层的精细控制机制仍然是未知的。我们的分析表明，脂质和F-肌动蛋白结合蛋白Abp 1是肌动蛋白驱动的刚毛在果蝇的发展至关重要。结合遗传，细胞生物学和生化分析表明，Abp 1触发皮层Arp 2/3介导的肌动蛋白成核的复合物形成的疤痕在刚毛的发展。质膜相关的Abp 1亚池的作用突出了组成性膜锚定的Abp 1。这种功能获得性实验导致严重的分裂刚毛表型，这与刚毛长度呈负相关。这种表型依赖于瘢痕，但不依赖于WASP，并需要与瘢痕相互作用的Abp 1的SH 3结构域。引人注目的是，敲除abp 1导致缺陷，在微毛类和巨毛类刚毛的完整性。重要的是，Arp 2和疤痕缺陷苍蝇表现出相似的刚毛表型。果蝇的微chaopathy缺陷的Abp 1，Arp 2和疤痕功能有扭结，而黄蜂杂合子果蝇没有。电子显微镜分析显示，abp 1敲除，Arp 2 RNAi和Scar RNAi都导致了扭曲的大刚毛与过多的脊。有趣的是，尽管Abp 1与瘢痕的物理关联及其使用Arp 2/3复合物激活剂作为效应物的能力，但abp 1敲除并不影响瘢痕的稳定性。这与经典的疤痕复合体成分（如Kette或Sra-1）形成对比。我们的工作表明，Abp 1是一个重要的，疤痕相互作用的因素控制皮质Arp 2/3介导的肌动蛋白成核和解开一个新的层的复杂性在感觉器官形成过程中皮质肌动蛋白成核的scopy控制。
Many developmental processes rely on cortical actin dynamics; however, the mechanisms of its fine control at the cell cortex are still largely unknown. Our analyses demonstrate that the lipid-and F-actin-binding protein Abp1 is crucial for actin-driven bristle development in Drosophila melanogaster. Combined genetic, cell biological and biochemical analyses reveal that Abp1 triggers cortical Arp2/3-mediated actin nucleation by complex formation with Scar in bristle development. The role of the plasma-membrane-associated Abp1 subpool was highlighted by constitutively membrane-anchored Abp1. Such gain-of-function experiments led to a severe split-bristle phenotype, which was negatively correlated with bristle length. This phenotype was dependent on Scar but not on WASP and required the Scar-interacting SH3 domain of Abp1. Strikingly, knockout of abp1 led to defects in both microchaete and macrochaete bristle integrity. Importantly, Arp2- and Scar-deficient flies displayed similar bristle phenotypes. Microchaetes of flies deficient for Abp1, Arp2 and Scar functions had kinks, whereas those of wasp heterozygous flies did not. Electron microscopy analyses revealed that abp1 knockout, Arp2 RNAi and Scar RNAi all led to distorted macrochaetes with an excessive number of ridges. Interestingly, despite the physical association of Abp1 with Scar and its ability to use the Arp2/3 complex activator as an effector, abp1 knockout did not affect Scar stability. This is in contrast to classical Scar complex components, such as Kette or Sra-1. Our work reveals that Abp1 is an important, Scar-interacting factor controlling cortical Arp2/3-mediated actin nucleation and unravels a novel layer of complexity in the scrupulous control of cortical actin nucleation during sensory organ formation.