MRC Laboratory of Molecular Biology, Cambridge Biomedical Campus, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3DY, UK.
Dev Cell. 2014 Jun 9;29(5):562-576. doi: 10.1016/j.devcel.2014.03.023.
The cytoskeleton is a major determinant of cell-shape changes that drive the formation of complex tissues during development. Important roles for actomyosin during tissue morphogenesis have been identified, but the role of the microtubule cytoskeleton is less clear. Here, we show that during tubulogenesis of the salivary glands in the fly embryo, the microtubule cytoskeleton undergoes major rearrangements, including a 90° change in alignment relative to the apicobasal axis, loss of centrosomal attachment, and apical stabilization. Disruption of the microtubule cytoskeleton leads to failure of apical constriction in placodal cells fated to invaginate. We show that this failure is due to loss of an apical medial actomyosin network whose pulsatile behavior in wild-type embryos drives the apical constriction of the cells. The medial actomyosin network interacts with the minus ends of acentrosomal microtubule bundles through the cytolinker protein Shot, and disruption of Shot also impairs apical constriction.
细胞骨架是决定细胞形状变化的主要因素,这种变化驱动着胚胎发育过程中复杂组织的形成。肌动球蛋白在组织形态发生过程中起着重要作用,但微管细胞骨架的作用则不太清楚。在这里,我们发现,在果蝇胚胎唾液腺的管状形成过程中,微管细胞骨架发生了重大重排,包括相对于顶底轴的 90°排列变化、中心体附着的丧失以及顶端的稳定。微管细胞骨架的破坏导致注定要内陷的基板细胞的顶端收缩失败。我们表明,这种失败是由于失去了一个顶端中部的肌动球蛋白网络,该网络在野生型胚胎中的脉动行为驱动了细胞的顶端收缩。中部肌动球蛋白网络通过细胞连接蛋白 Shot 与无中心体的微管束的负端相互作用,Shot 的破坏也会损害顶端收缩。