Dorsal closure during Drosophila embryogenesis provides a robust genetic platform to study the basic cellular mechanisms that govern epithelial wound healing and morphogenesis. As dorsal closure proceeds, the lateral epithelial tissue (LE) adjacent to the dorsal opening advance contra-laterally, with a simultaneous retraction of the amnioserosa. The process involves a fair degree of coordinated cell shape changes in the dorsal most epithelial (DME) cells as well as a few penultimate rows of lateral epithelial (LE) cells (collectively referred here as Dorsolateral Epithelial (DLE) cells), lining the periphery of the amnioserosa, which in due course of time extend contra-laterally and ultimately fuse over the dorsal hole, giving rise to a dorsal epithelial continuum. The JNK-Dpp signaling in the dorsolateral epidermis, plays an instrumental role in guiding their fate during this process. A large array of genes have been reported to be involved in the regulation of this core signaling pathway, yet the mechanisms by which they do so is hitherto unclear, which forms the objective of our present study. Here we show a probable mechanism via which lgl, a conserved tumour suppressor gene, regulates the JNK–Dpp pathway during dorsal closure and epithelial morphogenesis. A conditional/targeted knock-down of lgl in the dorsolateral epithelium of embryos results in failure of dorsal closure. Interestingly, we also observed a similar phenotype in a Rab11 knockdown condition. Our experiment suggests Rab11 to be interacting with lgl as they seem to synergize in order to regulate the core JNK-Dpp signaling pathway during dorsal closure and also during adult thorax closure process.

果蝇期间背闭合胚胎发生为研究控制上皮伤口愈合和形态发生的基本细胞机制提供了一个强大的遗传平台。随着背闭合的进行，与背开口相邻的外侧上皮组织（LE）向对侧推进，同时羊膜隆起。该过程涉及背侧最上皮（DME）细胞以及少数倒数第二排外侧上皮（LE）细胞（在此统称为背外侧上皮（DLE）细胞）中相当程度的协调细胞形状变化在适当的时间过程中，羊膜的对侧延伸并最终融合在背孔上，从而形成背上皮连续体。背外侧表皮中的JNK-Dpp信号传导 在引导他们命运的过程中起着重要作用。据报道，有大量基因参与了该核心信号通路的调控，但迄今为止，其调控机制尚不清楚，这构成了本研究的目标。这里我们展示了一种可能的机制lgl是一种保守的肿瘤抑制基因，在背侧闭合和上皮形态发生过程中调节JNK-Dpp途径。胚胎背外侧上皮中lgl的条件/靶向敲除会导致背侧闭合失败。有趣的是，我们还观察到了Rab11基因敲低条件下的相似表型。我们的实验表明，Rab11似乎与lgl相互作用，因为它们似乎协同作用，以便在闭合背以及成人胸腔闭合过程中调节核心JNK-Dpp信号通路。