Morphogenetic apoptosis : a force generation mechanism. Magali Suzanne, Melanie Gettings, Bruno Monier, Thomas Mangeat. Paul Sabatier University, LBCMCP, Toulouse, France.

   Apoptosis is involved in many crucial morphogenetic processes. However the question remains as to how dying cells influence their neighbors in order to drive tissue remodeling. We are currently investigating the role of apoptosis in the formation of Drosophila leg-joint, structures that separate each leg segment. We are focusing on the first morphogenetic event taking place during joint formation, which correspond to the folding of an epithelial tissue at the origin of adult leg, the leg disc. The analysis of cell shape organization revealed that cells in the presumptive joint are significantly stretched and aligned during fold formation. This suggests two things: the potential existence of a cellular boundary on one hand, and a discrepancy in cellular actin-myosin based tension between cells at the presumptive joint and cell within a leg segment on the other hand. The existence of a restriction boundary was confirmed by clone analysis and the cellular tension has been characterized by laser ablation, revealing a higher tension in a ring of cells at the future joint. We further observed that the apoptotic domain coincide with this stretched domain. These data suggested that the ring domain of higher tension observed in the fold is formed by the combination of a restriction boundary at the presumptive joint and a localized cell death. Analysis of cell shape in the absence of apoptosis indicates that cells are aligned but no longer stretched, suggesting that apoptosis induces cell stretching. The restriction of cell death by a physical boundary would ensures cell stretching rather than cell rearrangement. Thus the loss of cells through apoptosis would be compensated by cell stretching in order to maintain epithelial integrity. Thus, we hypothesize that the presence of a boundary is required at the presumptive joint to convert the elimination of cells into a morphogenetic driving force.