NUCLEAR RETENTION OF LEPTIN/UPD2 REGULATES ORGANISMAL RESILIENCE TO NUTRIENT EXTREMES

Abstract

AbstractAdipokines released from the adipocytes function as a systemic adipometer; they impinge on neural circuits to signal nutrient status. On starvation, adipokines must be retained to signal energy deficit; else, it significantly reduces starvation survival. But how fat cells retain adipokines is unclear. Here, we demonstrate that Atg8, a cell-intrinsic autophagy factor, regulates the starvation-induced acute retention of the Leptin Drosophila ortholog Upd2. We show that on starvation, as a direct consequence of Atg8’s lipidation, Upd2 accumulates in the nucleus. We illustrate that Upd2’s nuclear retention is critical to fat mobilization and increased starvation resilience. In conclusion, we propose that, during starvation, Atg8’s role is not just limited to autophagy but is critical for withholding adipokines in the nucleus to promote starvation resilience.