European Molecular Biology Laboratory (EMBL) Heidelberg, 69117 Heidelberg, Germany.
J Cell Biol. 2014 May 12;205(3):395-408. doi: 10.1083/jcb.201309079. Epub 2014 May 5.
Remodeling of cell shape during morphogenesis is driven by the coordinated expansion and contraction of specific plasma membrane domains. Loss of this coordination results in abnormal cell shape and embryonic lethality. Here, we show that plasma membrane lipid composition plays a key role in coordinating plasma membrane contraction during expansion. We found that an increase in PI(4,5)P2 levels caused premature actomyosin contraction, resulting in the formation of shortened cells. Conversely, acute depletion of PI(4,5)P2 blocked plasma membrane expansion and led to premature actomyosin disassembly. PI(4,5)P2-mediated contractility is counteracted by PI(3,4,5)P3 and the zygotic gene bottleneck, which acts by limiting myosin recruitment during plasma membrane expansion. Collectively, these data support a model in which the ratio of PI(4,5)P2/PI(3,4,5)P3 coordinates actomyosin contractility and plasma membrane expansion during tissue morphogenesis, thus ensuring proper cell shape.
在形态发生过程中,细胞形状的重塑是由特定质膜区域的协调扩展和收缩驱动的。这种协调的丧失会导致细胞形状异常和胚胎致死。在这里,我们表明质膜脂质组成在协调扩展过程中的质膜收缩中起着关键作用。我们发现,PI(4,5)P2 水平的增加导致肌动球蛋白的过早收缩,从而形成缩短的细胞。相反,PI(4,5)P2 的急性耗竭阻止了质膜的扩展,并导致肌动球蛋白的过早解体。PI(4,5)P2 介导的收缩性受到 PI(3,4,5)P3 和合子基因瓶颈的抑制,其作用是在质膜扩展期间限制肌球蛋白的募集。总之,这些数据支持这样一种模型,即 PI(4,5)P2/PI(3,4,5)P3 的比例协调肌动球蛋白的收缩性和质膜的扩展,从而确保适当的细胞形状。