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A WAVE2-Arp2/3 actin nucleator apparatus supports junctional tension at the epithelial zonula adherens

机译:WAVE2-Arp2 / 3肌动蛋白成核器设备支持上皮小带粘附的连接张力

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摘要

The epithelial zonula adherens (ZA) is a specialized adhesive junction where actin dynamics and myosin-driven contractility coincide. The junctional cytoskeleton is enriched in myosin II, which generates contractile force to support junctional tension. It is also enriched in dynamic actin filaments, which are replenished by ongoing actin assembly. In this study we sought to pursue the relationship between actin assembly and junctional contractility. We demonstrate that WAVE2-Arp2/3 is a major nucleator of actin assembly at the ZA and likely acts in response to junctional Rac signaling. Furthermore, WAVE2-Arp2/3 is necessary for junctional integrity and contractile tension at the ZA. Maneuvers that disrupt the function of either WAVE2 or Arp2/3 reduced junctional tension and compromised the ability of cells to buffer side-to-side forces acting on the ZA. WAVE2-Arp2/3 disruption depleted junctions of both myosin IIA and IIB, suggesting that dynamic actin assembly may support junctional tension by facilitating the local recruitment of myosin.
机译:上皮小带粘附(ZA)是一种特殊的粘附连接,肌动蛋白动力学与肌球蛋白驱动的收缩力重合。连接细胞骨架富含肌球蛋白II,它产生收缩力以支持连接张力。它也富含动态肌动蛋白丝,可以通过正在进行的肌动蛋白组装来补充。在这项研究中,我们试图探讨肌动蛋白组装和连接收缩之间的关系。我们证明WAVE2-Arp2 / 3是在ZA的肌动蛋白大会的主要成核剂,并可能响应联结Rac信号。此外,对于ZA处的连接完整性和收缩张力,WAVE2-Arp2 / 3是必需的。破坏WAVE2或Arp2 / 3功能的操纵降低了连接张力,并削弱了细胞缓冲作用在ZA上的左右力的能力。 WAVE2-Arp2 / 3破坏了肌球蛋白IIA和IIB的连接,表明动态肌动蛋白组装可通过促进肌球蛋白的局部募集来支持连接张力。

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