Abstract
Populations of proliferating cells such as stem cells and tumors are often nutrient responsive. Highly conserved signaling pathways communicate information about the surrounding environmental, organismal, and cellular nutrient conditions. One such pathway is the Target of Rapamycin (TOR) pathway. The TOR kinase exists in two complexes, TOR complex 1 (TORC1) and TOR complex 2 (TORC2). TORC1 has been researched extensively and its regulation, particularly by amino acids, is well characterized. TORC1 activity promotes both stem cell fate and proliferation in the Caenorhabditis elegans hermaphrodite germline stem cell system to facilitate expansion of the larval germline Progenitor Zone (PZ) pool in response to nutrients. By contrast, a role for TORC2 in germline development has not been investigated. Here, we show that RICT-1, the sole ortholog of the TORC2-specific component RICTOR, also promotes expansion of the larval PZ, acting largely through SGK-1. Further, unlike the germline-autonomous role for TORC1 components, intestinal rict-1 is both necessary and sufficient for full germline PZ pool establishment. Furthermore, neither DAF-2/IIS nor DAF-7/TGF-ß pathways mediate the effects of RICT-1. Rather, intestinal RICT-1 likely acts via vitellogenins, intestinally produced yolk proteins previously characterized for provisioning the adult germ line, but not previously characterized for a role in larval germ line development. By comparative RNA-seq on staged L4 larvae, we found vitellogenin genes among highly differentially abundant mRNAs. Genetic analysis supports a role for vit-3 in germline development in a linear pathway with rict-1. Our results establish the C. elegans germ line as a fruitful model for investigating TORC2 and its connection to stem cells and lipid biology.