C. elegans hedgehog/patched-like morphogen-receptor pair GRD-1/PTR-11 modulates developmental rate.

Both Hedgehog (Hh) and target of rapamycin complex 2 (TORC2) are central, evolutionarily conserved signaling 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, and grd-1/ptr-11 overexpression delays wild-type development similar to TORC2 loss of function animals. These findings potentially indicate an unexpected role for grd-1/ptr-11 in slowing developmental rate downstream of a nutrient sensing pathway. 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 TORC2 and grd-1/ptr-11 may act linearly or converge on pqm-1 to delay organismal development.