Open AccessJNK signaling in insulin‐producing cells is required for adaptive responses to stress in Drosophila
Author(s) -
Karpac Jason,
HullThompson Julie,
Falleur Melody,
Jasper Heinrich
Publication year - 2009
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/j.1474-9726.2009.00476.x
Subject(s) - psychological repression , biology , insulin , anabolism , adaptation (eye) , microbiology and biotechnology , oxidative stress , signal transduction , kinase , gene , insulin receptor , genetics , endocrinology , gene expression , insulin resistance , neuroscience
Summary 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.