JNK signaling in insulin-producing cells is required for adaptive responses to stress in Drosophila.
Adaptation to environmental challenges is critical for the survival of an organism. Repression of Insulin/IGF Signaling (IIS) by stress-responsive Jun-N-terminal Kinase (JNK) signaling is emerging as a conserved mechanism that allows reallocating resources from anabolic to repair processes under stress conditions. JNK activation in Insulin-producing cells (IPCs) is sufficient to repress Insulin and Insulin-like peptide (ILP) expression in rats and flies, but the significance of this interaction for adaptive responses to stress is unclear. In this study, it is shown that JNK activity in IPCs of flies is required for oxidative stress-induced repression of the Drosophila ILP2. It is found that this repression is required for growth adaptation to heat stress as well as adult oxidative stress tolerance, and that induction of stress response genes in the periphery is in part dependent on IPC-specific JNK activity. Endocrine control of IIS by JNK in IPCs is thus critical for systemic adaptation to stress.
Karpac
Jason
J
Department of Biology, University of Rochester, River Campus Box 270211, Rochester, NY 14627, USA.
Hull-Thompson
Julie
J
Falleur
Melody
M
Jasper
Heinrich
H
D000222:Adaptation, Physiological; D000818:Animals; D004330:Drosophila / Q000201:enzymology* / Q000254:growth & development; D029721:Drosophila Proteins / Q000378:metabolism; D050417:Insulin-Secreting Cells / Q000201:enzymology*; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism*; D020935:MAP Kinase Signaling System; D009479:Neuropeptides; D018384:Oxidative Stress; D013312:Stress, Physiological
D029721:Drosophila Proteins; C544178:ILP2 protein, Drosophila; D009479:Neuropeptides; D048031:JNK Mitogen-Activated Protein Kinases