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J. Biol. Chem., Vol. 280, Issue 18, 17732-17736, May 6, 2005
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Spatial Distribution of Di- and Tri-methyl Lysine 36 of Histone H3 at Active Genes*
¶**
From the
Wellcome Trust/Cancer Research UK Gurdon Institute and Department of Pathology, Tennis Court Road, Cambridge, CB2 1QN, United Kingdom, the ¶Max Planck Institute for Immunbiology, 79108 Freiburg, Germany, and the ||Biophysics Laboratories, Institute of Biomedical and Biomolecular Sciences, University of Portsmouth, Portsmouth PO1 2DT, United Kingdom
Methylation of lysine 4 of histone H3 (K4/H3) is linked to transcriptional activity, whereas methylation of K9/H3 is tightly associated with gene inactivity. These are well characterized sites of methylation within histones, but there are numerous other, less characterized, sites of modification. In Saccharomyces cerevisiae, methylation of K36/H3 has been linked to active genes, but little is known about this methylation in higher eukaryotes. Here we analyzed for the first time the levels and spatial distribution of di- and tri-methyl (di- and tri-Me) K36/H3 in metazoan genes. We analyzed chicken genes that are developmentally regulated, constitutively active, or inactive. We found that active genes contain high levels of these modifications compared with inactive genes. Furthermore, in actively transcribed regions the levels of di- and tri-Me K36/H3 peak toward the 3' end of the gene. This is in striking contrast to the distributions of di- and tri-Me K4/H3, which peak early in actively transcribed regions. Thus, di/tri-Me K4/H3 and di/tri-Me K36/H3 are both useful markers of active genes, but their genic distribution indicates differing roles. Our data suggest that the unique spatial distribution of di- and tri-Me K36/H3 plays a role in transcriptional termination and/or early RNA processing.
Received for publication, January 21, 2005 , and in revised form, March 9, 2005.
* This work was supported by Cancer Research UK and European Union Grant QLG1-CT-2000-01935 (to T. K. laboratory) and by Biotechnology and Biological Sciences Research Council (to C. C.-R. laboratory). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
These authors contributed equally.
** To whom correspondence should be addressed: Wellcome Cancer Research UK Gurdon Institute, Tennis Ct. Rd., Cambridge CB2 1QN, UK. Tel.: 44-1223-334112; Fax: 44-1223-334089; E-mail: tk106{at}mole.bio.cam.ac.uk.
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