Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisboa, Portugal.
PLoS One. 2011;6(9):e23964. doi: 10.1371/journal.pone.0023964. Epub 2011 Sep 16.
Coordination of apical constriction in epithelial sheets is a fundamental process during embryogenesis. Here, we show that DRhoGEF2 is a key regulator of apical pulsation and constriction of amnioserosal cells during Drosophila dorsal closure. Amnioserosal cells mutant for DRhoGEF2 exhibit a consistent decrease in amnioserosa pulsations whereas overexpression of DRhoGEF2 in this tissue leads to an increase in the contraction time of pulsations. We probed the physical properties of the amnioserosa to show that the average tension in DRhoGEF2 mutant cells is lower than wild-type and that overexpression of DRhoGEF2 results in a tissue that is more solid-like than wild-type. We also observe that in the DRhoGEF2 overexpressing cells there is a dramatic increase of apical actomyosin coalescence that can contribute to the generation of more contractile forces, leading to amnioserosal cells with smaller apical surface than wild-type. Conversely, in DRhoGEF2 mutants, the apical actomyosin coalescence is impaired. These results identify DRhoGEF2 as an upstream regulator of the actomyosin contractile machinery that drives amnioserosa cells pulsations and apical constriction.
上皮细胞的顶端收缩协调是胚胎发生过程中的一个基本过程。在这里,我们表明 DRhoGEF2 是果蝇背闭过程中羊膜细胞顶端搏动和收缩的关键调节因子。羊膜细胞中 DRhoGEF2 的突变表现出羊膜搏动的一致减少,而在该组织中过表达 DRhoGEF2 导致搏动的收缩时间增加。我们探测了羊膜的物理性质,表明 DRhoGEF2 突变细胞的平均张力低于野生型,并且 DRhoGEF2 的过表达导致组织比野生型更固体状。我们还观察到,在 DRhoGEF2 过表达的细胞中,顶端肌动球蛋白聚合并发显著增加,这可能有助于产生更多的收缩力,导致羊膜细胞的顶端表面积比野生型小。相反,在 DRhoGEF2 突变体中,顶端肌动球蛋白聚合并发受损。这些结果表明 DRhoGEF2 是驱动羊膜细胞搏动和顶端收缩的肌动球蛋白收缩机制的上游调节剂。