The Transcription Factor Myc Controls Metabolic Reprogramming upon T Lymphocyte Activation

To fulfill the bioenergetic and biosynthetic demand of proliferation, T cells reprogram their metabolic pathways from fatty acid β-oxidation and pyruvate oxidation via the TCA cycle to the glycolytic, pentose-phosphate, and glutaminolytic pathways. Two of the top-ranked candidate transcription facto...

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Veröffentlicht in:Immunity (Cambridge, Mass.) Mass.), 2011-12, Vol.35 (6), p.871-882
Hauptverfasser: Wang, Ruoning, Dillon, Christopher P., Shi, Lewis Zhichang, Milasta, Sandra, Carter, Robert, Finkelstein, David, McCormick, Laura L., Fitzgerald, Patrick, Chi, Hongbo, Munger, Joshua, Green, Douglas R.
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container_issue 6
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container_title Immunity (Cambridge, Mass.)
container_volume 35
creator Wang, Ruoning
Dillon, Christopher P.
Shi, Lewis Zhichang
Milasta, Sandra
Carter, Robert
Finkelstein, David
McCormick, Laura L.
Fitzgerald, Patrick
Chi, Hongbo
Munger, Joshua
Green, Douglas R.
description To fulfill the bioenergetic and biosynthetic demand of proliferation, T cells reprogram their metabolic pathways from fatty acid β-oxidation and pyruvate oxidation via the TCA cycle to the glycolytic, pentose-phosphate, and glutaminolytic pathways. Two of the top-ranked candidate transcription factors potentially responsible for the activation-induced T cell metabolic transcriptome, HIF1α and Myc, were induced upon T cell activation, but only the acute deletion of Myc markedly inhibited activation-induced glycolysis and glutaminolysis in T cells. Glutamine deprivation compromised activation-induced T cell growth and proliferation, and this was partially replaced by nucleotides and polyamines, implicating glutamine as an important source for biosynthetic precursors in active T cells. Metabolic tracer analysis revealed a Myc-dependent metabolic pathway linking glutaminolysis to the biosynthesis of polyamines. Therefore, a Myc-dependent global metabolic transcriptome drives metabolic reprogramming in activated, primary T lymphocytes. This may represent a general mechanism for metabolic reprogramming under patho-physiological conditions. [Display omitted] ► T cell activation drives the transcription of a distinct set of metabolic genes ► Myc is required for activation-induced metabolic reprogramming ► HIF1 is not required for activation-induced metabolic reprogramming ► Myc-driven glutaminolysis fuels polyamine biosynthesis upon T cell activation
doi_str_mv 10.1016/j.immuni.2011.09.021
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[Display omitted] ► T cell activation drives the transcription of a distinct set of metabolic genes ► Myc is required for activation-induced metabolic reprogramming ► HIF1 is not required for activation-induced metabolic reprogramming ► Myc-driven glutaminolysis fuels polyamine biosynthesis upon T cell activation</description><identifier>ISSN: 1074-7613</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/j.immuni.2011.09.021</identifier><identifier>PMID: 22195744</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Bioenergetics ; Cell activation ; Cell cycle ; Cell growth ; Cell proliferation ; Fatty acids ; Gene expression ; Gene Expression Regulation ; Glucose - metabolism ; Glutamine ; Glutamine - metabolism ; Glycolysis ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Kinases ; Lymphocyte Activation - genetics ; Lymphocytes T ; Metabolic Networks and Pathways - genetics ; Metabolic pathways ; Metabolites ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myc protein ; Nucleotides ; Ornithine - metabolism ; Oxidation ; polyamines ; Polyamines - metabolism ; Proto-Oncogene Proteins c-myc - genetics ; Proto-Oncogene Proteins c-myc - metabolism ; Pyruvic acid ; T-Lymphocytes - immunology ; T-Lymphocytes - metabolism ; TOR Serine-Threonine Kinases - metabolism ; Tracers ; Transcription factors ; Transcriptome ; Tricarboxylic acid cycle</subject><ispartof>Immunity (Cambridge, Mass.), 2011-12, Vol.35 (6), p.871-882</ispartof><rights>2011 Elsevier Inc.</rights><rights>Copyright © 2011 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Dec 23, 2011</rights><rights>2011 Elsevier Inc. All rights reserved. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c523t-52e1ec90cd561cb52be2857cd2a9bc0f002abeb27062c2e806a4bf875f8cfb063</citedby><cites>FETCH-LOGICAL-c523t-52e1ec90cd561cb52be2857cd2a9bc0f002abeb27062c2e806a4bf875f8cfb063</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1074761311005152$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22195744$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Ruoning</creatorcontrib><creatorcontrib>Dillon, Christopher P.</creatorcontrib><creatorcontrib>Shi, Lewis Zhichang</creatorcontrib><creatorcontrib>Milasta, Sandra</creatorcontrib><creatorcontrib>Carter, Robert</creatorcontrib><creatorcontrib>Finkelstein, David</creatorcontrib><creatorcontrib>McCormick, Laura L.</creatorcontrib><creatorcontrib>Fitzgerald, Patrick</creatorcontrib><creatorcontrib>Chi, Hongbo</creatorcontrib><creatorcontrib>Munger, Joshua</creatorcontrib><creatorcontrib>Green, Douglas R.</creatorcontrib><title>The Transcription Factor Myc Controls Metabolic Reprogramming upon T Lymphocyte Activation</title><title>Immunity (Cambridge, Mass.)</title><addtitle>Immunity</addtitle><description>To fulfill the bioenergetic and biosynthetic demand of proliferation, T cells reprogram their metabolic pathways from fatty acid β-oxidation and pyruvate oxidation via the TCA cycle to the glycolytic, pentose-phosphate, and glutaminolytic pathways. 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[Display omitted] ► T cell activation drives the transcription of a distinct set of metabolic genes ► Myc is required for activation-induced metabolic reprogramming ► HIF1 is not required for activation-induced metabolic reprogramming ► Myc-driven glutaminolysis fuels polyamine biosynthesis upon T cell activation</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22195744</pmid><doi>10.1016/j.immuni.2011.09.021</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record>
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subjects Animals
Bioenergetics
Cell activation
Cell cycle
Cell growth
Cell proliferation
Fatty acids
Gene expression
Gene Expression Regulation
Glucose - metabolism
Glutamine
Glutamine - metabolism
Glycolysis
Hypoxia-Inducible Factor 1, alpha Subunit - metabolism
Kinases
Lymphocyte Activation - genetics
Lymphocytes T
Metabolic Networks and Pathways - genetics
Metabolic pathways
Metabolites
Mice
Mice, Inbred C57BL
Mice, Knockout
Myc protein
Nucleotides
Ornithine - metabolism
Oxidation
polyamines
Polyamines - metabolism
Proto-Oncogene Proteins c-myc - genetics
Proto-Oncogene Proteins c-myc - metabolism
Pyruvic acid
T-Lymphocytes - immunology
T-Lymphocytes - metabolism
TOR Serine-Threonine Kinases - metabolism
Tracers
Transcription factors
Transcriptome
Tricarboxylic acid cycle
title The Transcription Factor Myc Controls Metabolic Reprogramming upon T Lymphocyte Activation
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