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Compelling evidence has also revealed that altered metabolic energetics in HSCs underlies the onset of certain blood diseases; however, the mechanisms responsible for energetic reprogramming remain elusive. We recently found that Fanconi anemia (FA) HSCs in their resting state are more dependent on mitochondrial respiration for energy metabolism than on glycolysis. In the present study, we investigated the role of deficient glycolysis in FA HSC maintenance. We observed significantly reduced glucose consumption, lactate production, and ATP production in HSCs but not in the less primitive multipotent progenitors or restricted hematopoietic progenitors of Fanca\u2212\/\u2212 and Fancc\u2212\/\u2212 mice compared with that of wild-type mice, which was associated with an overactivated p53 and TP53-induced glycolysis regulator, the TIGAR-mediated metabolic axis. We utilized Fanca\u2212\/\u2212 HSCs deficient for p53 to show that the p53-TIGAR axis suppressed glycolysis in FA HSCs, leading to enhanced pentose phosphate pathway and cellular antioxidant function and, consequently, reduced DNA damage and attenuated HSC exhaustion. Furthermore, by using Fanca\u2212\/\u2212 HSCs carrying the separation-of-function mutant p53R172P transgene that selectively impairs the p53 function in apoptosis but not cell-cycle control, we demonstrated that the cell-cycle function of p53 was not required for glycolytic suppression in FA HSCs. Finally, ectopic expression of the glycolytic rate-limiting enzyme PFKFB3 specifically antagonized p53-TIGAR-mediated metabolic reprogramming in FA HSCs. Together, our results suggest that p53-TIGAR metabolic axis-mediated glycolytic suppression may play a compensatory role in attenuating DNA damage and proliferative exhaustion in FA HSCs. Stem Cells \u00a02019;37:937\u2013947<\/jats:p>\n               <jats:sec>\n                  <jats:title\/>\n               <\/jats:sec>","DOI":"10.1002\/stem.3015","type":"journal-article","created":{"date-parts":[[2019,4,12]],"date-time":"2019-04-12T11:48:20Z","timestamp":1555069700000},"page":"937-947","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["p53-TP53-Induced Glycolysis Regulator Mediated Glycolytic Suppression Attenuates DNA Damage and Genomic Instability in Fanconi Anemia Hematopoietic Stem Cells"],"prefix":"10.1093","volume":"37","author":[{"given":"Xue","family":"Li","sequence":"first","affiliation":[{"name":"a Department of Pharmaceutical Sciences, School of Pharmacy, West Virginia University, Morgantown, West Virginia, USA"},{"name":"b Institute for Brain Research and Rehabilitation, South China Normal University, Guangzhou, People's Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Limei","family":"Wu","sequence":"additional","affiliation":[{"name":"a Department of Pharmaceutical Sciences, School of Pharmacy, West Virginia University, Morgantown, West Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Morgan","family":"Zopp","sequence":"additional","affiliation":[{"name":"a Department of Pharmaceutical Sciences, School of Pharmacy, West Virginia University, Morgantown, West Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shaina","family":"Kopelov","sequence":"additional","affiliation":[{"name":"a Department of Pharmaceutical Sciences, School of Pharmacy, West Virginia University, Morgantown, West Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3669-537X","authenticated-orcid":false,"given":"Wei","family":"Du","sequence":"additional","affiliation":[{"name":"a Department of Pharmaceutical Sciences, School of Pharmacy, West Virginia University, Morgantown, West Virginia, USA"},{"name":"c Alexander B. Osborn Hematopoietic Malignancy and Transplantation Program, West Virginia University Cancer Institute, Morgantown, West Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2019,5,3]]},"reference":[{"key":"2022022514405572600_stem3015-bib-0001","doi-asserted-by":"crossref","first-page":"68","DOI":"10.1097\/00062752-200301000-00011","article-title":"Genetic basis of Fanconi anemia","volume":"10","author":"Bagby","year":"2003","journal-title":"Curr Opin Hematol"},{"key":"2022022514405572600_stem3015-bib-0002","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1136\/jmg.40.1.1","article-title":"Fanconi anaemia","volume":"40","author":"Tischkowitz","year":"2003","journal-title":"J Med Genet"},{"key":"2022022514405572600_stem3015-bib-0003","doi-asserted-by":"crossref","first-page":"3580","DOI":"10.1172\/JCI88010","article-title":"Biallelic inactivation of REV7 is associated with Fanconi 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