Dihydroxyacetone phosphate generated in the chloroplast mediates the activation of TOR by CO₂ and light.

Abstract

Light and CO₂ assimilation activate the target of rapamycin (TOR) kinase in photosynthetic cells, but how these signals are transmitted to TOR is unknown. Using the green alga <i>Chlamydomonas reinhardtii</i> as a model system, we identified dihydroxyacetone phosphate (DHAP) as the key metabolite regulating TOR in response to carbon and light cues. Metabolomic analyses of synchronized cells revealed that DHAP levels change more than any other metabolite between dark- and light-grown cells and that the addition of the DHAP precursor, dihydroxyacetone (DHA), was sufficient to activate TOR in the dark. We also demonstrated that TOR was insensitive to light or inorganic carbon but not to exogenous DHA in a <i>Chlamydomonas</i> mutant defective in the export of DHAP from the chloroplast. Our results provide a metabolic basis for the mode of TOR control by light and inorganic carbon and indicate that cytoplasmic DHAP is an important metabolic regulator of TOR.