GSE196384
Genome wide transcriptional change by  GPR155/LYCHOS  loss
Cholesterol, a key building block for cellular membranes and a precursor for steroid hormones, was recently identified as a major nutrient input that activates the master growth regulator, mammalian Target of Rapamycin Complex 1 (mTORC1) kinase. Here we identify a novel lysosomal tranmembrane protein , which we name LYsosomal CHOlesterol Signaling (LYCHOS, previously annotated as GPR155/DEPDC3), as an essential factor that enables cholesterol-dependent activation of mTORC1. RNAseq analysis of LYCHOS-depleted cells showed a pronounced dowregulation of  metabolic genes involved in glycolysis, pentose phosphate pathway and lipid biosynthesis. Overall design: HEK293T cells  were infected with lentivirus <shLuc+ FLAG METAP2>, <shLYCHOS + FLAG METAP2> and <shLYCHOS + LYCHOS WT FLAG>  and  RNA was extracted 5 days post-infection and analyzed by RNA-sequencing