Intestinal RICT-1/Rictor regulates larval germline progenitors via vitellogenins VIT-1 and VIT-3 in C. elegans

Abstract

Highly conserved signaling pathways communicate cellular and organismal nutrient conditions to proliferating pools of cells such as stem cells and tumors. 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). In the Caenorhabditis elegans hermaphrodite, TORC1 signaling cell-autonomously promotes the establishment of the larval germline Progenitor Zone (PZ). Here, we show that RICT-1, the sole C. elegans ortholog of the TORC2-specific component Rictor, also promotes expansion of the larval PZ through canonical TORC2 signaling. Unlike the TORC1 components, intestinal rict-1 is both necessary and sufficient for full germline PZ pool establishment. Comparative RNA-seq on staged L4 larvae indicates that intestinal RICT-1 likely acts via vitellogenins. These intestinally produced yolk proteins provision oocytes, but they were not previously known to act in larval germ line development. Genetic analysis supports roles for vit-1 and vit-3 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. Summary StatementRICT-1/Rictor in C. elegans promotes larval germline development via canonical TORC2 signaling, and intestinal RICT-1 acts via vitellogenins VIT-1 and VIT-3 to promote the establishment of the germline progenitor pool.