期刊
SCIENCE
卷 324, 期 5929, 页码 930-935出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1170116
关键词
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资金
- NIH [AI44432, K08 HL089150]
- a Scholar Award from the Juvenile Diabetes Research Foundation
- Harvard Stem Cell Institute [Seed]
- Howard Hughes Medical Institute
- NIH/NIGMS [R01GM065865]
- American Heart Association postdoctoral fellowship
- National Library of Medicine, NIH
- Lady Tata Memorial postdoctoral fellowship
- NSF Graduate Fellowships
- Department of Defense graduate fellowship
DNA cytosine methylation is crucial for retrotransposon silencing and mammalian development. In a computational search for enzymes that could modify 5-methylcytosine (5mC), we identified TET proteins as mammalian homologs of the trypanosome proteins JBP1 and JBP2, which have been proposed to oxidize the 5-methyl group of thymine. We show here that TET1, a fusion partner of the MLL gene in acute myeloid leukemia, is a 2-oxoglutarate (2OG)- and Fe(II)-dependent enzyme that catalyzes conversion of 5mC to 5-hydroxymethylcytosine (hmC) in cultured cells and in vitro. hmC is present in the genome of mouse embryonic stem cells, and hmC levels decrease upon RNA interference-mediated depletion of TET1. Thus, TET proteins have potential roles in epigenetic regulation through modification of 5mC to hmC.
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