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Status |
Public on Sep 01, 2022 |
Title |
Genome wide transcriptional change by GPR155/LYCHOS loss |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
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.
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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
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Contributor(s) |
Shin HR, Zoncu R |
Citation(s) |
36007018 |
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Submission date |
Feb 08, 2022 |
Last update date |
Dec 01, 2022 |
Contact name |
Roberto Zoncu |
E-mail(s) |
rzoncu@berkeley.edu
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Organization name |
University of California Berkeley
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Department |
Molecular Cell Biology
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Street address |
Li Ka Shing Center, 1951 Oxford Street, Rm330F
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City |
Berkeley |
State/province |
California |
ZIP/Postal code |
94720 |
Country |
USA |
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Platforms (1) |
GPL24676 |
Illumina NovaSeq 6000 (Homo sapiens) |
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Samples (6)
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Relations |
BioProject |
PRJNA804551 |