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This article is part of the supplement: Epigenetics and Chromatin: Interactions and processes

Open Access Oral presentation

Chromatin modifications and dynamics during repair of a double-strand chromosome break in budding yeast

James E Haber1*, Cheng-Sheng Lee1, Kihoon Lee1, Michael Tsabar1, Wade Hicks1 and Gaelle Legube2

  • * Corresponding author: James E Haber

Author Affiliations

1 Rosenstiel Center and Department of Biology, Brandeis University, Waltham MA 02454, USA

2 Université de Toulouse, UPS, LBCMCP, Toulouse, France

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Epigenetics & Chromatin 2013, 6(Suppl 1):O16  doi:10.1186/1756-8935-6-S1-O16


The electronic version of this article is the complete one and can be found online at: http://www.epigeneticsandchromatin.com/content/6/S1/O16


Published:18 March 2013

© 2013 Haber et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Oral presentation

A single double-strand break (DSB) triggers the ATR/ATM (Mec1/Tel1)-dependent DNA damage response in budding yeast. These kinases phosophorylate not only histone H2A (γ-H2AX) but also the C-terminal threonine of histone H2B (γ-H2B), both of which contribute to checkpoint responses and repair of the DSB. Despite both being phosphorylated by the same kinases, γ-H2AX kinetics are much more rapid than that of γ-H2B, but when H2A is mutated to prevent its phosphorylation, γ-H2B kinetics adopt the rapid kinetics seen for γ-H2AX. Both modifications are removed the PP4 phosphatase. γ-H2AX and γ-H2B spread over ≥ 50 kb on either side of the DSB but they are nearly absent in strongly transcribed regions. When transcription is turned off, γ-H2AX rises to a high level within 10 min, catalyzed by either Mec1 or Tel1, even 5 h after the break was induced and when Tel1 is reported no longer to be associated with the DSB. We show that if a DSB is created within 15 kb of one yeast centromere that γ-H2AX and γ-H2B spread to the pericentromeric regions of all other chromosomes, demonstrating that the kinases can act in trans to regions of DNA that are located in close proximity.

When a DSB is created in a locus that can be repaired by gene conversion, 5’ to 3’ resection leads to the loss of well-positioned nucleosomes adjacent to the DSB. When repair is complete, nucleosomes are re-established, but the pattern is distinct from that seen prior to the break or when the repaired cells are allowed to replicate. Chromatin re-establishment is dependent on the histone chaperones CAF-1 and Asf1.