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Molecular and Cellular Biology, December 2006, p. 9185-9195, Vol. 26, No. 24
0270-7306/06/$08.00+0     doi:10.1128/MCB.01529-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Profile of Histone Lysine Methylation across Transcribed Mammalian Chromatin{triangledown} ,{dagger}

Christopher R. Vakoc,1,2 Mira M. Sachdeva,2 Hongxin Wang,1 and Gerd A. Blobel1,2*

The Children's Hospital of Philadelphia, Division of Hematology, Philadelphia, Pennsylvania 19104,1 University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 191042

Received 16 August 2006/ Returned for modification 21 September 2006/ Accepted 27 September 2006

Complex patterns of histone lysine methylation encode distinct functions within chromatin. We previously reported that trimethylation of lysine 9 of histone H3 (H3K9) occurs at both silent heterochromatin and at the transcribed regions of active mammalian genes, suggesting that the extent of histone lysine methylation involved in mammalian gene activation is not completely defined. To identify additional sites of histone methylation that respond to mammalian gene activity, we describe here a comparative assessment of all six known positions of histone lysine methylation and relate them to gene transcription. Using several model loci, we observed high trimethylation of H3K4, H3K9, H3K36, and H3K79 in the transcribed region, consistent with previous findings. We identify H4K20 monomethylation, a modification previously linked with repression, as a mark of transcription elongation in mammalian cells. In contrast, H3K27 monomethylation, a modification enriched at pericentromeric heterochromatin, was observed broadly distributed throughout all euchromatic sites analyzed, with selective depletion in the vicinity of the transcription start sites at active genes. Together, these results underscore that similar to other described methyl-lysine modifications, H4K20 and H3K27 monomethylation are versatile and dynamic with respect to gene activity, suggesting the existence of novel site-specific methyltransferases and demethylases coupled to the transcription cycle.

* Corresponding author. Mailing address: Abramson Pediatric Research Center, The Children's Hospital of Philadelphia, 3615 Civic Center Blvd., Philadelphia, PA 19104. Phone: (215) 590-3988. Fax: (215) 590-4834. E-mail: blobel{at}email.chop.edu.

{triangledown} Published ahead of print on 9 October 2006.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, December 2006, p. 9185-9195, Vol. 26, No. 24
0270-7306/06/$08.00+0     doi:10.1128/MCB.01529-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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