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Using Abelson transformed pre\u2013B cell lines, we find that H2AX is not required for coding join formation within chromosomal V(D)J recombination substrates. Yet we show that H2AX is phosphorylated along cleaved Ig\u03ba DNA strands and prevents their separation in G1 phase cells and their progression into chromosome breaks and translocations after cellular proliferation. We also show that H2AX prevents chromosome breaks emanating from unrepaired RAG endonuclease-generated TCR-\u03b1\/\u03b4 locus coding ends in primary thymocytes. Our data indicate that histone H2AX suppresses translocations during V(D)J recombination by creating chromatin modifications that stabilize disrupted antigen receptor locus DNA strands to prevent their irreversible dissociation. We propose that such H2AX-dependent mechanisms could function at additional chromosomal locations to facilitate the joining of DNA ends generated by other types of DSBs.<\/jats:p>","DOI":"10.1084\/jem.20091320","type":"journal-article","created":{"date-parts":[[2009,11,3]],"date-time":"2009-11-03T02:35:55Z","timestamp":1257215755000},"page":"2625-2639","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":50,"title":["Histone H2AX stabilizes broken DNA strands to suppress chromosome breaks and translocations during V(D)J recombination"],"prefix":"10.1084","volume":"206","author":[{"given":"Bu","family":"Yin","sequence":"first","affiliation":[{"name":"Cell and Molecular Biology Graduate Group 1 , 2 , and 3"},{"name":"Abramson Family Cancer Research Institute 1 , 2 , and 3"},{"name":"Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 1 , 2 , and 3"},{"name":"Cell and Molecular Biology 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