Abstract
Mei-P26 is associated with cell-fate regulation in Drosophila melanogaster . In prior work, offspring of Western diet-fed fathers exhibited hyperphagia accompanied by increased brain Mei-P26. Because feeding is regulated by insulin/ILP signaling, we tested whether altering mei-p26 expression in insulin-producing cells affects behavioral and metabolic outcomes. Here we show that overexpression of mei-p26 in ILP2 neurons reduced feeding (FLIC), consumption (ConEx), locomotor activity, and glucose levels by 30-50%, whereas mei-p26 knockdown produced opposite effects. These effects were consistent across sexes, identifying Mei-P26 as a potential regulator within insulin-producing cells associated with bidirectional changes in adult behavioral and metabolic readouts.
