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The Journal of Immunology, 2002, 169: 3094-3104.
Copyright © 2002 by The American Association of Immunologists

Variable Diversity Joining Recombination: Nonhairpin Coding Ends in Thymocytes of SCID and Wild-Type Mice1

Pamela B. Nakajima2 and Melvin J. Bosma

Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, PA 19111

Initiation of V(D)J recombination results in broken DNA molecules with blunt recombination signal ends and covalently sealed (hairpin) coding ends. In SCID mice, coding joint formation is severely impaired and hairpin coding ends accumulate as a result of a deficiency in the catalytic subunit of DNA-dependent protein kinase, an enzyme involved in the repair of DNA double-strand breaks. In this study, we report that not all SCID coding ends are hairpinned. We have detected open J{delta}1 and D{delta}2 coding ends at the TCR{delta} locus in SCID thymocytes. Approximately 25% of 5'D{delta}2 coding ends were found to be open. Large deletions and abnormally long P nucleotide additions typical of SCID D{delta}2-J{delta}1 coding joints were not observed. Most J{delta}1 and D{delta}2 coding ends exhibited 3' overhangs, but at least 20% had unique 5' overhangs not previously detected in vivo. We suggest that the SCID DNA-dependent protein kinase deficiency not only reduces the efficiency of hairpin opening, but also may affect the specificity of hairpin nicking, as well as the efficiency of joining open coding ends.




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