The evolutionarily conserved target-of-rapamycin (TOR) kinase controls fundamental metabolic processes to support cell growth. TOR functions within the context of two distinct complexes, TORC1 and TORC2. The TORC2 with its specific component Rictor has been recently implicated in aging and regulation of growth and metabolism. Here, we identify
rict-1/Rictor as a new regulator of embryonic development in C. elegans. The transcription factor
skn-1 is essential to establish the development of the mesendoderm in embryos and is required for cellular homeostasis and longevity in adult worms. Loss of
skn-1 function in the embryo leads to mis-specification of the mesendodermal precursor consequently lacking intestine and pharynx. We found that genetic inactivation of
rict-1 re-stored mesendodermal specification in
skn-1 deficient embryos and thereby suppressed
skn-1-associated lethality. Moreover, inactivation of the TORC2 components but not TORC1 partially rescued
skn-1 embryonic lethality. SGK-1 mediated these functions downstream of
rict-1/TORC2 as a
sgk-1 gain of function mutant suppressed the
rict-1 mutant phenotype. These data indicate that TORC2 and SGK-1 antagonize SKN-1 during embryonic development.