The biosynthesis of isoprenoids in plant cells occurs from precursors produced in the cytosol by the mevalonate(MVA) pathway and in the plastid by the methylerythritol 4-phosphate(MEP) pathway,but little is known about the mechanisms coordinating both pathways.Evidence of the importance of sugar signaling for such coordination in Arabidopsis thaliana is provided here by the characterization of a mutant showing an increased accumulation of MEP-derived isoprenoid products(chlorophylls and carotenoids) without changes in the levels of relevant MEP pathway transcripts,proteins,or enzyme activities.This mutant was found to be a new loss-of-function allele of PRL1(Pleiotropic Regulatory Locus 1) ,a gene encoding a conserved WD-protein that functions as a global regulator of sugar,stress,and hormone responses,in part by inhibition of SNF1-related protein K_(in) ases(SnRK1).Consistent with the reported role of SnRK1 K_(in) ases in the phosphorylation and inactivation of the main regulatory enzyme of the MVA pathway(hydroxymethylglutaryl coenzyme-A reductase) ,its activity but not transcript or protein levels was reduced in prl1 seedlings.However,the accumulation of MVA-derived end products(sterols) was unaltered in mutant seedlings.Sucrose supplementation to wildtype seedlings phenocopied the prl1 mutation in terms of isoprenoid metabolism,suggesting that the observed isoprenoid phenotypes result from the increased sugar accumulation in the prl1 mutant.In summary,PRL1 appears to coordinate isoprenoid metabolism with sugar,hormone,and stress responses.