Nervous system cells can be expose to a wide range of stress conditions, such as infection, hypoxia or DNA damaged by ionizing radiation (IR). Cells can response to stressful stimuli in various ways, from the activation of survival pathways, to the induction of apoptosis that eventually eliminates damaged cells. When insults result in neural damage, a regenerative response aims to preserve the structural integrity and function of the nervous system is induced. Glial cells mediate this response. Therefore, understanding the underlying mechanisms that control glial response after damage in terms of first, number and cell types, and secondly, signalling pathways that control their response, is key for developing strategies to repair the damaged tissue.

Although our knowledge about the genetic factors promoting glial regenerative response has greatly improved over the past decade, there are still many important issues about this process that remains largely unknown. To obtain a complete understanding of how these processes are regulated, it is essential to use model organisms that allow us in vivo studies, in the context of the complex interactions that take place among the different cell types that are involved. To address these issues, we take advantage of the unique developmental features of the Drosophila eye imaginal disc.

As we mentioned above, nerve cells can respond differently to the same stressful stimulus. Our results indicate that glial cells, and also some neuroblasts, do not die after IR. This result suggests that, either the apoptotic pathway is blocked in these cells, or the stress response induced by genotoxicity is not sufficient to activate the apoptotic pathway. Our goal is to define the genetic and molecular mechanisms that block or attenuate the apoptotic response to IR in these cells. This is relevant for understanding the mechanisms that confer high intrinsic resistance of glioma cells to irradiation.