Apical deficiency triggers JNK-dependent apoptosis in the embryonic epidermis of Drosophila

• DOI: 10.1242/dev.059980
• Publication Date: 2011-06-21T11:44:10Z
• Authors: Golnar Kolahgar; Pierre-Luc Bardet; Paul F. Langton; Cyrille Alexandre; Jean-Paul Vincent
• Keywords: 0303 health sciences; Gene Expression Profiling; JNK Mitogen-Activated Protein Kinases; Gene Expression Regulation, Developmental; Apoptosis; Adherens Junctions; Microarray Analysis; 03 medical and health sciences; Epidermal Cells; Phosphoprotein Phosphatases; Animals; Drosophila Proteins; Drosophila; Epidermis; In Situ Hybridization; Signal Transduction

Epithelial homeostasis and the avoidance of diseases such as cancer require the elimination of defective cells by apoptosis. Here, we investigate how loss of apical determinants triggers apoptosis in the embryonic epidermis of Drosophila. Transcriptional profiling and in situ hybridisation show that JNK signalling is upregulated in mutants lacking Crumbs or other apical determinants. This leads to transcriptional activation of the pro-apoptotic gene reaper and to apoptosis. Suppression of JNK signalling by overexpression of Puckered, a feedback inhibitor of the pathway, prevents reaper upregulation and apoptosis. Moreover, removal of endogenous Puckered leads to ectopic reaper expression. Importantly, disruption of the basolateral domain in the embryonic epidermis does not trigger JNK signalling or apoptosis. We suggest that apical, not basolateral, integrity could be intrinsically required for the survival of epithelial cells. In apically deficient embryos, JNK signalling is activated throughout the epidermis. Yet, in the dorsal region, reaper expression is not activated and cells survive. One characteristic of these surviving cells is that they retain discernible adherens junctions despite the apical deficit. We suggest that junctional integrity could restrain the pro-apoptotic influence of JNK signalling.