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Molecular and Cellular Biology, January 2008, p. 71-82, Vol. 28, No. 1
0270-7306/08/$08.00+0     doi:10.1128/MCB.01534-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

The Transcriptional Status but Not the Imprinting Control Region Determines Allele-Specific Histone Modifications at the Imprinted H19 Locus{triangledown}

Raluca I. Verona, Joanne L. Thorvaldsen, Kimberly J. Reese, and Marisa S. Bartolomei*

Department of Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104

Received 22 August 2007/ Returned for modification 15 September 2007/ Accepted 11 October 2007

Genomic imprinting governs allele-specific gene expression in an epigenetically heritable manner. The characterization of histone modifications at imprinted gene loci is incomplete, and whether specific histone marks determine transcription or are dependent on it is not understood. Using chromatin immunoprecipitations, we examined in multiple cell types and in an allele-specific manner the active and repressive histone marks of several imprinted loci, including H19, KvDMR1, Snrpn promoter/exon 1, and IG-DMR imprinting control regions. Expressed alleles are enriched for specific actively modified histones, including H3 di- and trimethylated at Lys4 and acetylated histones H3 and H4, while their silent counterparts are associated with repressive marks such as H3 trimethylated at Lys9 alone or in combination with H3 trimethylated at Lys27 and H4/H2A symmetrically dimethylated at Arg3. At H19, allele-specific histone modifications occur throughout the entire locus, including nontranscribed regions such as the differentially methylated domain (DMD) as well as sequences in the H19 gene body that are not differentially methylated. Significantly, the presence of active marks at H19 depends on transcriptional activity and occurs even in the absence of the DMD. These findings suggest that histone modifications are dependent on the transcriptional status of imprinted alleles and illuminate epigenetic mechanisms of genomic imprinting.

* Corresponding author. Mailing address: Department of Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104. Phone: (215) 898-9063. Fax: (215) 573-6434. E-mail: bartolom{at}mail.med.upenn.edu

{triangledown} Published ahead of print on 29 October 2007.

Molecular and Cellular Biology, January 2008, p. 71-82, Vol. 28, No. 1
0270-7306/08/$08.00+0     doi:10.1128/MCB.01534-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Koerner, M. V., Pauler, F. M., Huang, R., Barlow, D. P. (2009). The function of non-coding RNAs in genomic imprinting. Development 136: 1771-1783 [Abstract] [Full Text]  
  • Engel, N., Raval, A. K., Thorvaldsen, J. L., Bartolomei, S. M. (2008). Three-dimensional conformation at the H19/Igf2 locus supports a model of enhancer tracking. Hum Mol Genet 17: 3021-3029 [Abstract] [Full Text]  
  • Singh, V., Srivastava, M. (2008). Enhancer Blocking Activity of the Insulator at H19-ICR Is Independent of Chromatin Barrier Establishment. Mol. Cell. Biol. 28: 3767-3775 [Abstract] [Full Text]  


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