Karkali Katerina, Pastor-Pareja Jose Carlos, Martin-Blanco Enrique
Instituto de Biologia Molecular de Barcelona, Consejo Superior de Investigaciones Científicas (IBMB-CSIC), Barcelona, Spain.
Instituto de Neurociencias, Consejo Superior de Investigaciones Científicas (IN-CSIC), Alicante, Spain.
Front Cell Dev Biol. 2024 Jan 9;11:1034484. doi: 10.3389/fcell.2023.1034484. eCollection 2023.
The fusion of epithelial sheets is an essential and conserved morphogenetic event that requires the maintenance of tissue continuity. This is secured by membrane-bound or diffusible signals that instruct the epithelial cells, in a coordinated fashion, to change shapes and adhesive properties and when, how and where to move. Here we show that during Dorsal Closure (DC) in the Jun kinase (JNK) signaling pathway modulates integrins expression and ensures tissue endurance. An excess of JNK activity, as an outcome of a failure in the negative feedback implemented by the dual-specificity phosphatase Puckered (Puc), promotes the loss of integrins [the ß-subunit Myospheroid (Mys)] and amnioserosa detachment. Likewise, integrins signal back to the pathway to regulate the duration and strength of JNK activity. Mys is necessary for the regulation of JNK activity levels and in its absence, expression is downregulated and JNK activity increases.
上皮细胞层的融合是一个基本且保守的形态发生事件，需要维持组织的连续性。这通过膜结合或可扩散信号得以确保，这些信号以协调的方式指示上皮细胞改变形状和黏附特性，以及何时、如何以及向何处移动。在这里，我们表明在背侧闭合（DC）过程中，Jun激酶（JNK）信号通路调节整合素的表达并确保组织的耐受性。由于双特异性磷酸酶褶皱（Puc）实施的负反馈失败，过量的JNK活性会促进整合素[β亚基肌球样蛋白（Mys）]的丧失和羊膜浆膜脱离。同样，整合素会反向作用于该信号通路，以调节JNK活性的持续时间和强度。Mys对于调节JNK活性水平是必需的，在其缺失时，表达会下调且JNK活性会增加。
