Journal
DEVELOPMENTAL CELL
Volume 56, Issue 19, Pages 2692-+Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2021.09.010
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Funding
- NIH [P40OD010440]
- National Key R&D Program of China [2019YFA0802804]
- National Natural Science Foundation of China [32170837, 92057107]
- Recruitment Program of Global Experts of China (Youth)
- Shanghai Pujiang Program [16PJ1407400]
- ShanghaiTech Startup program
- Ministry of Science and Technology of China [2019YFA0802503]
- Collaborative Innovation Program of Shanghai Municipal Health Commission [2020CXJQ01]
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This study identified a lipid biosynthesis pathway that mediates amino acid sensing in the intestine and neuronal mTORC1, affecting development by regulating protein translation and ribosomal biogenesis. Findings suggest a similar mechanism may operate in mammals, providing new insights into the role of amino acid sensing mechanisms in animals.
Animals have developed various nutrient-sensing mechanisms for survival under fluctuating environmental conditions. Although extensive cell-culture-based analyses have identified diverse mediators of amino acid sensing upstream of mTOR, studies using animal models to examine intestine-initiated amino acid sensing mechanisms under specific physiological conditions are lacking. Here, we developed a Caenorhabditis elegans model to examine the impact of amino acid deficiency on development. We discovered a leucine-derived monomethyl branched-chain fatty acid and its downstream metabolite, glycosphingolipid, which critically mediates the overall amino acid sensing by intestinal and neuronal mTORC1, which in turn regulates postembryonic development at least partly by controlling protein translation and ribosomal biogenesis. Additional data suggest that a similar mechanism may operate in mammals. This study uncovers an amino-acid-sensing mechanism mediated by a lipid biosynthesis pathway.
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