ABSTRACT
Both Hedgehog (Hh) signaling and target of rapamycin complex 2 (TORC2) are central, evolutionarily conserved pathways that regulate development and metabolism. In C. elegans, loss of essential TORC2 component RICTOR (rict-1) causes delayed development, shortened lifespan, reduced brood, small size, and increased fat. Here we report that knockdown of Hedgehog-related morphogen grd-1 and its Patched-related receptor ptr-11 rescues delayed development in TORC2 loss of function mutants, indicating an unexpected role for grd-1/ptr-11 in slowing developmental rate downstream of nutrient sensing pathways. Further, we implicate chronic stress transcription factor pqm-1 as a key transcriptional effector of grd-1/ptr-11 in slowing whole-organism growth. We propose that the TORC2/grd-1/ptr-11/pqm-1 signaling relay acts as a critical executor of growth to slow development when C. elegans encounters unfavorable growth conditions.
Summary statement Developmental rate in C. elegans is dramatically slowed in animals deficient in nutrient-sensitive target of rapamycin complex 2 signaling and slowing is effected by increased activity of a previously uncharacterized Hh-r/Ptr signaling relay.
Competing Interest Statement
The authors have declared no competing interest.
