Tissue regeneration is widespread among animal species. Following cell death, regeneration requires compensatory proliferation of the surviving cells to replace lost cells. I use the Drosophila wing imaginal disc in order to address the spatio-temporal regulation of regeneration following cell death with single cell resolution. I transiently express the pro-apoptotic gene reaper in clones and I show that cell proliferation is not locally increased around dying clones, but rather globally upregulated on the level of the whole tissue. This burst of proliferation is transient and resolves within ten hours after the end of death induction. Interestingly, adult wing size is not affected, indicating that compensatory proliferation ensures the robustness of development after cell death. To further study the link between compensatory proliferation and developmental robustness, I transiently induce cell death in the anterior compartment of the wing disc. I show that after an initial loss of tissue proportions between the anterior and posterior compartments, there is a partial recovery of proportions after an increase in proliferation at larval stage. Interestingly, tissue proportions are not fully recovered in the adult wing, while total wing size is rescued, indicating uncoupling between tissue size and shape. I am currently investigating the nature of the pro-proliferative signal (mechanics/secreted factors) giving rise to compensatory proliferation. Furthermore, since cell death occurs in cell competition, I wish to determine the contribution of compensatory proliferation to winner cell expansion and tissue invasion. I show that winner clones grow more in the presence of loser (Discs large-depleted) clones. Similar to clone apoptosis, I do not observe a local increase in proliferation of winner clones in proximity to loser clones. I am currently investigating whether winner and loser cells have a different sensitivity to compensatory signals, which could be a novel mechan
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