Understanding roles of calcium signalling in apoptosis-induced proliferation

Apoptosis is a well-conserved, regulated form of cell death which can be activated in response to stress and damage. This process is mediated by caspases, which execute or initiate apoptosis. However, caspases also have non-apoptotic functions. One of which is to drive apoptosis-induced proliferation (AiP). AiP is a compensatory mechanism in which stress-induced dying cells emit signals to trigger proliferation of their neighbouring cells. AiP has been observed in multiple organisms including mammals and it has been shown to play important roles in tissue regeneration. Where AiP is chronic and uncontrolled, it can result in tissue overgrowth. Therefore, deciphering the regulation of AiP, at the cellular and molecular level, has implications for our understanding of tissue regeneration and growth control. This project will explore roles of calcium signalling, a cellular process essential for wound healing and regeneration, in the regulation of AiP by using Drosophila melanogaster as a model organism.