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Published online 29 March 2004

Nucleic Acids Research, 2004, Vol. 32, No. 6 1942-1947
© 2004 Oxford University Press

Histone 3 lysine 4 methylation during the pre-B to immature B-cell transition

Eric J. Perkins1, Barbara L. Kee4 and Dale A. Ramsden*,1,2,3

1 Curriculum in Genetics and Molecular Biology, 2 Lineberger Comprehensive Cancer Center and 3 Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, NC 27599, USA and 4 University of Chicago, Department of Pathology and Committee on Immunology, 5841 S. Maryland Avenue, MC 1089, IL 60637, USA

*To whom correspondence should be addressed at Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, NC 27599, USA. Tel: +1 919 966 9809; Fax: +1 919 966 3015; Email: dale_ramsden{at}med.unc.edu

Received January 23, 2004; Revised and Accepted March 10, 2004

The relationship between chromatin modification and lymphocyte development is still poorly understood. Here we show a correlation between methylation of lysine 4 on histone 3 (H3-K4) and activation of several loci required for the pre-B cell to immature B-cell developmental transition. A critical step in this transition is the induction of V(D)J recombination at the Ig{kappa} locus. Upon activation of Ig{kappa} recombination, a >10-fold enrichment of both di- and trimethylated H3-K4 is observed at J{kappa} targeting signals, but not at an analogous targeting signal in the T-cell receptor {alpha} locus or, surprisingly, at several V{kappa} signals. However, H3-K4 methylation is restricted to the actively recombining fraction of J{kappa} recombination targeting signals, consistent with a direct relationship between H3-K4 methylation and signal activity. Correlations between increased H3-K4 methylation and induction of transcription are also observed at some, but not all, loci where transcription is induced. H3-K4 methylation may therefore be a widely used but not universal means for controlling chromatin activity in this developmental transition.


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