223C Poster - 01. Cell Stress and cell death
Saturday April 09, 1:30 PM - 3:30 PM

Authors:
Morgan Mutch; Jiaqi Chen; Denise Montell

Affiliation: University of California, Santa Barbara

Keywords:
h. other (Apoptosis); h. other (Apoptosis)

The regulation of cell death and survival is critical for tissue development and function. Our lab has characterized a process named ‘anastasis,’ which is defined as cell survival following executioner caspase activation, previously thought to be the irreversible marker of apoptosis. Anastasis has been found to function during development, oncogenesis, and cell survival following injury in a variety of animal and cell culture models. Most anastasis research has focused on mammalian cancer cell lines and fly epithelial tissue, both highly proliferative cell types. However, the significance of anastasis has yet to be determined in the nervous system. Post-mitotic neurons have been shown to initiate apoptosis and activate executioner caspases without executing apoptosis in a neurodegenerative disease model. We propose that anastasis might enhance survival of neurons following stress like human Tau expression where it might function to slow neurodegeneration. I performed a loss of function screen in D. melanogaster photoreceptor neurons to test the functions of genes that affect anastasis in proliferating wing imaginal discs for effects on neurodegeneration. The results suggest that the Insulin Receptor/Akt pathway, which drives cell proliferation, enhances Tau toxicity in the Tau-induced rough-eye model. I am currently investigating how Tau interacts with the Insulin Receptor/Akt pathway in fly photoreceptors, and how expression of signaling components changes Akt activity in a Tau background. In addition, I am exploring the role of Insulin Receptor signaling in regulating anastasis and apoptosis in a neurodegeneration model. I will present progress in understanding anastasis and genetic regulators of neurodegeneration in the fly nervous system.