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Identify cellular responses to decreased SAMe production
Our studies in C. elegans showed that SREBP transcriptional activators could control expression 1CC genes. These studies are important because they demonstrate that levels of these critical enzymes mRNAa are not controlled as a “housekeeping function” but are instead are coordinated with other cellular processes. We have developed two models for 1CC dysfunction in C. elegans, a genetic model based on loss of function (lof) of sams-1, a SBP-1/SREBP responsive gene encoding the enzyme for producing the methyl donor SAMe and a dietary model in which C. elegans are fed bacteria unable to synthesize folate. In both of these models, transcription of lipogenic genes are highly increased and sams-1(lof) worms accumulate large lipid droplets, mimicking aspects of fatty liver disease in mammals. These models will allow use genetic screens as a tool for identifying 1) other regulatory pathways affecting SAMe production or utilization and 2) cellular responses that limit lipogenesis when methyl donor levels are low.