Brodu Véronique, Casanova Jordi
Institut de Biologia Molecular de Barcelona (CSIC) and Institut de Recerca Biomèdica, Parc Científic de Barcelona, 08028 Barcelona, Spain.
Genes Dev. 2006 Jul 1;20(13):1817-28. doi: 10.1101/gad.375706.
A major issue in morphogenesis is to understand how the activity of genes specifying cell fate affects cytoskeletal components that modify cell shape and induce cell movements. Here, we approach this question by investigating how a group of cells from an epithelial sheet initiate invagination to ultimately form the Drosophila tracheal tubes. We describe tracheal cell behavior at invagination and show that it is associated with, and requires, a distinct recruitment of Myosin II to the apical surface of cells at the invaginating edge. We show that this process is achieved by the activity of crossveinless-c, a gene coding for a RhoGAP and whose specific transcriptional activation in the tracheal cells is triggered by both the trachealess patterning gene and the EGF Receptor (EGFR) signaling pathway. Our results identify a developmental pathway linking cell fate genes and cell signaling pathways to intracellular modifications during tracheal cell invagination.
形态发生中的一个主要问题是了解决定细胞命运的基因活性如何影响细胞骨架成分,这些成分会改变细胞形状并诱导细胞运动。在这里,我们通过研究上皮层中的一组细胞如何启动内陷以最终形成果蝇气管来探讨这个问题。我们描述了气管细胞在内陷时的行为,并表明这与肌球蛋白II向正在内陷边缘的细胞顶端表面的独特募集有关,并且需要这种募集。我们表明,这个过程是由无横脉c的活性实现的,无横脉c是一种编码RhoGAP的基因,其在气管细胞中的特异性转录激活由气管缺失模式基因和表皮生长因子受体(EGFR)信号通路共同触发。我们的结果确定了一条发育途径,该途径将细胞命运基因和细胞信号通路与气管细胞内陷过程中的细胞内修饰联系起来。