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A correction to this article has been published: Wang et al., J. Exp. Med. 203 (2) 473
Published online 17 January 2006 doi:10.1084/jem.20051774
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 1, 215-226
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ARTICLE

 AID-dependent histone acetylation is detected in immunoglobulin S regions

Lili Wang, Naree Whang, Robert Wuerffel, and Amy L. Kenter

Department of Microbiology and Immunology, University of Illinois College of Medicine, Chicago, IL 60612

CORRESPONDENCE Amy L. Kenter: star1{at}uic.edu

Class switch recombination (CSR) is regulated by the expression of activation-induced deaminase (AID) and germline transcripts (GLTs). AID-dependent double-strand breaks (DSBs) are introduced into switch (S) regions and stimulate CSR. Although histone acetylation (Ac) has been well documented in transcription regulation, its role in DNA damage repair remains largely unexplored. The 1B4.B6 B cell line and normal splenic B cells were activated to undergo CSR and analyzed for histone Ac by chromatin immunoprecipitation (ChIP). A detailed study of the I{gamma}3-S{gamma}3-C{gamma}3 locus demonstrated that acetylated histones are focused to the I{gamma}3 exon and the S{gamma}3 region but not to the intergenic areas. Histone H3 Ac is strongly correlated with GLT expression at four S regions, whereas H4 Ac was better associated with B cell activation and AID expression. To more directly examine the relationship between H4 Ac and AID, LPS-activated AID KO and WT B cells were analyzed and express comparable levels of GLTs. In AID-deficient B cells, both histones H3 and H4 are reduced where H4 is more severely affected as compared with WT cells. Our findings raise the intriguing possibility that histone H4 Ac at S regions is a marker for chromatin modifications associated with DSB repair during CSR.

Abbreviations used: Ac, acetylation; AID, activation-induced deaminase; CD40L, CD40 ligand; ChIP, chromatin immunoprecipitation; CSR, class switch recombination; DSB, double-strand break; GLT, germline transcript; NHEJ, nonhomologous end joining; P, promoter; q, quantitative; RPA, replication protein A; ss, single stranded; SHM, somatic hypermutation.


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