A novel gain-of-function mutation in sgk-1 partially suppresses mTORC2 defects.

Abstract

The serine/threonine protein kinase SGK-1 is a downstream target of mTOR complex 2 (mTORC2) and is a conserved regulator of growth and metabolism. In C. elegans , mutations in rict-1 , which encodes an essential component of mTORC2, impairs lipid homeostasis and growth; however, these defects are partially suppressed by an activating mutation in SGK-1 , E116K. Here, we describe a stronger gain-of-function mutation in sgk-1 , L112F, that was identified in a forward genetic screen for rict-1 suppressor mutations . This allele will be useful in further dissecting the mTORC2 pathway and provides new insight into the role of this conserved residue in regulating SGK-1 kinase activity.