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通过利用预先存在的肌动球蛋白收缩来触发细胞形状变化。

Triggering a cell shape change by exploiting preexisting actomyosin contractions.

机构信息

Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

出版信息

Science. 2012 Mar 9;335(6073):1232-5. doi: 10.1126/science.1217869. Epub 2012 Feb 9.

Abstract

Apical constriction changes cell shapes, driving critical morphogenetic events, including gastrulation in diverse organisms and neural tube closure in vertebrates. Apical constriction is thought to be triggered by contraction of apical actomyosin networks. We found that apical actomyosin contractions began before cell shape changes in both Caenorhabitis elegans and Drosophila. In C. elegans, actomyosin networks were initially dynamic, contracting and generating cortical tension without substantial shrinking of apical surfaces. Apical cell-cell contact zones and actomyosin only later moved increasingly in concert, with no detectable change in actomyosin dynamics or cortical tension. Thus, apical constriction appears to be triggered not by a change in cortical tension, but by dynamic linking of apical cell-cell contact zones to an already contractile apical cortex.

摘要

顶端缢缩改变细胞形状,驱动包括不同生物的原肠胚形成和脊椎动物的神经管闭合在内的关键形态发生事件。顶端缢缩被认为是由顶端肌动球蛋白网络的收缩引发的。我们发现,在秀丽隐杆线虫和果蝇中,细胞形状变化之前,顶端肌动球蛋白收缩就已经开始。在秀丽隐杆线虫中,肌动球蛋白网络最初是动态的,在没有明显缩小顶端表面的情况下收缩并产生皮质张力。随后,顶端细胞-细胞接触区和肌动球蛋白才越来越协调地移动,肌动球蛋白动力学或皮质张力没有明显变化。因此,顶端缢缩似乎不是由皮质张力的变化引发的,而是由顶端细胞-细胞接触区与已经收缩的顶端皮质的动态连接引发的。

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