Blog
About

930
views
0
recommends
+1 Recommend
0 collections
    40
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Conversion of 5-methylcytosine to 5-hydroxymethylcytosine in mammalian DNA by MLL partner TET1.

      Science (New York, N.Y.)

      Animals, Transfection, Sequence Alignment, RNA Interference, metabolism, genetics, chemistry, Proto-Oncogene Proteins, Molecular Sequence Data, Mice, Mass Spectrometry, Hydroxylation, Humans, Embryonic Stem Cells, Dinucleoside Phosphates, DNA-Binding Proteins, DNA Methylation, DNA, analysis, analogs & derivatives, Cytosine, Cell Line, Amino Acid Sequence, 5-Methylcytosine

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          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.

          Related collections

          Author and article information

          Journal
          19372391
          2715015
          10.1126/science.1170116

          Comments

          Comment on this article