H2AX Prevents DNA Breaks from Progressing to Chromosome Breaks and Translocations
Open accessAbstract
Histone H2AX promotes DNA double-strand break (DSB) repair and immunoglobulin heavy chain (IgH) class switch recombination (CSR) in B-lymphocytes. CSR requires activation-induced cytidine deaminase (AID) and involves joining of DSB intermediates by end joining. We find that AID-dependent IgH locus chromosome breaks occur at high frequency in primary H2AX-deficient B cells activated for CSR and that a substantial proportion of these breaks participate in chromosomal translocations. Moreover, activated B cells deficient for ATM, 53BP1, or MDC1, which interact with H2AX during the DSB response, show similarly increased IgH locus breaks and translocations. Thus, our findings implicate a general role for these factors in promoting end joining and thereby preventing DSBs from progressing into chromosomal breaks and translocations. As cellular p53 status does not markedly influence the frequency of such events, our results also have implications for how p53 and the DSB response machinery cooperate to suppress generation of lymphomas with oncogenic translocations.
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Unrepaired double-strand breaks progress to chromosomal breaks.
“Unrepaired double-strand breaks progress to chromosomal breaks (18), as we observed.”
From Mdm2 Promotes Genetic Instability and Transformation Independent of p53 (2008) · cites this paper as [18]
Histone H2AX is phosphorylated at serine 139 by ATM to form γ-H2AX, which prevents double-strand breaks from being processed into chromosomal translocations.
“As an ATM substrate, histone H2AX is phosphorylated at Serine 139, which is referred to γ-H2AX and prevents DSBs from processing into chromosomal translocations [58, 59].”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [59]
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- Authors
- Franco, S., Gostissa, M., Zha, S., Lombard, D. B., Murphy, M. M., Zarrin, A. A., Yan, C., Tepsuporn, S., Morales, J. C., Adams, M. M., Lou, Z., Bassing, C. H., Manis, J. P., Chen, J., Carpenter, P. B., & Alt, F. W.
- Affiliations
- Howard Hughes Medical Institute (US)
- Brigham and Women's Hospital (US)
- The University of Texas Health Science Center at Houston (US)
- Mayo Clinic (US)
- Children's Hospital of Philadelphia (US)
- Boston Children's Hospital (US)
- Corresponding author
- Alt, Frederick W.
- ORCID
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2006-01
- Volume
- 21
- Issue
- 2
- Pages
- 201-214
- ISSN
- 1097-2765 (ISSN-L)
- OpenAlex
- W2146355613
- Cited by
- 282
- References
- 60
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 2 · 2023: 5 · 2022: 7 · 2021: 6 · 2020: 11 · 2019: 3 · 2018: 6 · 2017: 9 · 2016: 13 · 2015: 16 · 2014: 18 · 2013: 21 · 2012: 12
- FWCI
- 14.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 2790 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Molecular Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (2PO1AI031541-15, CA92312, GM65812, PO1CA092625-05, RO1 CA89239)
- U.S. Department of Defense (DAMD17-02-1-0472, DAMD17-03-1-0610)
- European Molecular Biology Organization
- Leukemia and Lymphoma Society
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- histone H2AX, DNA double-strand break repair, activation-induced cytidine deaminase, chromosomal translocation, chromosome breakage, B cells, ATM, 53BP1, MDC1, p53, end-joining, lymphoma, DNA damage response
- MeSH terms
- AICDA (Activation-Induced Cytidine Deaminase), Animals, B-Lymphocytes, Cytidine Deaminase, DNA Damage, DNA Repair, Histones, Immunoglobulin Heavy Chains, Translocation, Genetic, Tumor Suppressor Protein p53, In Situ Hybridization, Fluorescence, Immunoglobulin Class Switching, Mice, Knockout, Chromosome Breakage, Mice, In Vitro Techniques
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