IRC3regulates mitochondrial translation in response to metabolic cues inSaccharomyces cerevisiae

Abstract

AbstractMitochondrial oxidative phosphorylation (OXPHOS) enzymes are made up of dual genetic origin. Mechanism regulating expression of nuclear encoded OXPHOS subunits in response to metabolic cues (glucose vs. glycerol), is significantly understood while regulation of mitochondrially encoded OXPHOS subunits is poorly defined. Here, we show thatIRC3a DEAD/H box helicase, previously implicated in mitochondrial DNA maintenance, is central to integrating metabolic cues with mitochondrial translation. Irc3 associates with mitochondrial small ribosomal subunit in cells consistent with its role in regulating translation elongation based on Arg8mreporter system. Glucose grownΔirc3ρ+andirc3temperature sensitive cells at 37⁰C have reduced translation rates from majority of mRNAs. In contrast, when galactose was the carbon source, reduction in mitochondrial translation was observed predominantly from Cox1 mRNA inΔirc3ρ+but no defect was observed inirc3temperature sensitive cells, at 37⁰C. In support, of a model wherebyIRC3responds to metabolic cues, suppressors of Δirc3isolated for restoration of growth on glycerol media restore mitochondrial translation differentially in presence of glucose vs. glycerol.