Abstract 3061 Control of IP3 receptor trafficking at the ER-mitochondrial contact sites

ER and mitochondria form close contacts (ERMCs) that are central to almost every aspects of cell function, including metabolism and signaling. ERMCs are dynamically restructured to meet the continuously changing demands of the cell, but how ERMCs are formed and dissolved is yet to be determined. We hypothesized that IP3Rs that locally transfer Ca2+ from the ER to the mitochondria also mediate ERMC formation in an isoform-specific and activation-dependent manner. We tested this hypothesis using a novel iLID-SspB-based optogenetic toolkit that enabled us to monitor the dynamics of the IP3Rs close to the mitochondria.