{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lu V"],"funding":["NICHD NIH HHS","NCI NIH HHS","NIGMS NIH HHS","NIH HHS"],"pagination":["610-623.e8"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8930616"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["57(5)"],"pubmed_abstract":["Human pluripotent stem cells (hPSCs) can self-renew indefinitely or can be induced to differentiate. We previously showed that exogenous glutamine (Gln) withdrawal biased hPSC differentiation toward ectoderm and away from mesoderm. We revealed that, although all three germ lineages are capable of de novo Gln synthesis, only ectoderm generates sufficient Gln to sustain cell viability and differentiation, and this finding clarifies lineage fate restrictions under Gln withdrawal. Furthermore, we found that Gln acts as a signaling molecule for ectoderm that supersedes lineage-specifying cytokine induction. In contrast, Gln in mesoderm and endoderm is the preferred precursor of α-ketoglutarate without a direct signaling role. Our work raises a question about whether the nutrient environment fun"],"journal":["Developmental cell"],"pubmed_title":["Glutamine-dependent signaling controls pluripotent stem cell fate."],"pmcid":["PMC8930616"],"funding_grant_id":["R01 GM127985","P30 CA016042","R01 GM073981","F31 HD097960","R21 CA227480","S10 OD025017"],"pubmed_authors":["Roy IJ","Ahsan FM","Lu V","Graham NA","Joly JH","Torres A","Teitell MA"],"additional_accession":[]},"is_claimable":false,"name":"Glutamine-dependent signaling controls pluripotent stem cell fate.","description":"Human pluripotent stem cells (hPSCs) can self-renew indefinitely or can be induced to differentiate. We previously showed that exogenous glutamine (Gln) withdrawal biased hPSC differentiation toward ectoderm and away from mesoderm. We revealed that, although all three germ lineages are capable of de novo Gln synthesis, only ectoderm generates sufficient Gln to sustain cell viability and differentiation, and this finding clarifies lineage fate restrictions under Gln withdrawal. Furthermore, we found that Gln acts as a signaling molecule for ectoderm that supersedes lineage-specifying cytokine induction. In contrast, Gln in mesoderm and endoderm is the preferred precursor of α-ketoglutarate without a direct signaling role. Our work raises a question about whether the nutrient environment fun","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Mar","modification":"2026-05-09T13:57:10.861Z","creation":"2025-02-19T00:13:12.709Z"},"accession":"S-EPMC8930616","cross_references":{"pubmed":["35216682"],"doi":["10.1016/j.devcel.2022.02.003"]}}