ATM stabilizes DNA double-strand-break complexes during V(D)J recombination

Nature

Volumn 442, Issue 7101, 2006, Pages 466-470

  Bredemeyer, Andrea L ^a   Sharma, Girdhar G ^a   Huang, Ching Yu ^a   Helmink, Beth A ^a   Walker, Laura M ^a   Khor, Katrina C ^a   Nuskey, Beth ^b   Sullivan, Kathleen E ^b   Pandita, Tej K ^a   Bassing, Craig H ^b,c   Sleckman, Barry P ^a  

^a WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b UNIVERSITY OF PENNSYLVANIA   (United States)

^c UNIVERSITY OF PENNSYLVANIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANTIGENS; CELLS; CHROMOSOMES; ENZYMES; GENES; PROTEINS; TUMORS;

ATAXIA-TELANGIECTASIA; CELL-CYCLE CHECKPOINT; CHROMOSOMAL DNA; LYMPHOID TUMOURS;

DNA;

ATM PROTEIN; DOUBLE STRANDED DNA; LYMPHOCYTE ANTIGEN RECEPTOR; CELL CYCLE PROTEIN; DNA BINDING PROTEIN; PROTEIN SERINE THREONINE KINASE; TUMOR SUPPRESSOR PROTEIN;

CELL ORGANELLE; DNA; METABOLISM; MUTATION; PROTEIN; RESPONSE ANALYSIS;

ANIMAL CELL; APOPTOSIS; ARTICLE; ATAXIA TELANGIECTASIA; CANCER SUSCEPTIBILITY; CELL CYCLE REGULATION; CHROMOSOME TRANSLOCATION; DNA DAMAGE; DNA RECOMBINATION; DNA REPAIR; DNA STRAND BREAKAGE; GENE LOCUS; GENOMIC INSTABILITY; LYMPHOCYTOPENIA; LYMPHOMA; MOUSE; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; PROTEIN FUNCTION; ANIMAL; B LYMPHOCYTE; CELL LINE; CHROMOSOME BREAKAGE; GENE REARRANGEMENT; GENETICS; METABOLISM; STEM CELL;

ATAXIA; ATAXIA TELANGIECTASIA;

ANIMALS; ATAXIA TELANGIECTASIA; B-LYMPHOCYTES; CELL CYCLE PROTEINS; CELL LINE; CHROMOSOME BREAKAGE; DNA DAMAGE; DNA REPAIR; DNA-BINDING PROTEINS; GENE REARRANGEMENT, B-LYMPHOCYTE; MICE; PROTEIN-SERINE-THREONINE KINASES; STEM CELLS; TUMOR SUPPRESSOR PROTEINS;

EID: 33747097562     PISSN: 00280836     EISSN: 14764687     Source Type: Journal    
DOI: 10.1038/nature04866     Document Type: Article

References (29)

1. Kastan, M. B. & Lim, D. S. The many substrates and functions of ATM. Nature Rev. Mol. Cell Biol. 1, 179-186 (2000).
2. Pandita, T. K. A multifaceted role for ATM in genome maintenance. Expert Rev. Mol. Med. 5, 1-21 (2003).
3. Shiloh, Y. ATM and related protein kinases: safeguarding genome integrity. Nature Rev. Cancer 3, 155-168 (2003).
4. Durocher, D. & Jackson, S. P. DNA-PK, ATM and ATR as sensors of DNA damage: variations on a theme? Curr. Opin. Cell Biol. 13, 225-231 (2001).
5. Lavin, M. F. & Shiloh, Y. The genetic defect in ataxia- telangiectasia. Annu. Rev. Immunol. 15, 177-202 (1997).
6. Taylor, A. M., Metcalfe, J. A., Thick, J. & Mak, Y. F. Leukemia and lymphoma in ataxia telangiectasia. Blood 87, 423-438 (1996).
7. Tonegawa, S. Somatic generation of antibody diversity. Nature 302, 575-581 (1983).
8. Fugmann, S. D., Lee, A. I., Shockett, P. E., Villey, I. J. & Schatz, D. G. The RAG proteins and V(D)J recombination: complexes, ends, and transposition. Annu. Rev. Immunol. 18, 495-527 (2000).
9. Oettinger, M. A. V(D)J recombination: on the cutting edge. Curr. Opin. Cell Biol. 11, 325-329 (1999).
10. Gellert, M. V(D)J recombination: rag proteins, repair factors, and regulation. Annu. Rev. Biochem. 71, 101-132 (2002).
11. Bassing, C. H. & Alt, F. W. The cellular response to general and programmed DNA double strand breaks. DNA Repair (Amst.) 3, 781-796 (2004).
12. Matei, I. R., Guidos, C. J. & Danska, J. S. ATM-dependent DNA damage surveillance in T-cell development and leukemogenesis: the DSB connection. Immunol. Rev. 209, 142-158 (2006).
13. Perkins, E. J. et al. Sensing of intermediates in V(D)J recombination by ATM. Genes Dev. 16, 159-164 (2002).
14. Liao, M. J. & Van Dyke, T. Critical role for Atm in suppressing V(D)J recombination-driven thymic lymphoma. Genes Dev. 13, 1246-1250 (1999).
15. Petiniot, L. K. et al. Recombinase-activating gene (RAG) 2-mediated V(D)J recombination is not essential for tumorigenesis in Atm-deficient mice. Proc. Natl Acad. Sci. USA 97, 6664-6669 (2000).
16. Donehower, L. A. et al. Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours. Nature 356, 215-221 (1992).
17. Hirao, A. et al. Chk2 is a tumor suppressor that regulates apoptosis in both an ataxia telangiectasia mutated (ATM)-dependent and an ATM-independent manner. Mol. Cell. Biol. 22, 6521-6532 (2002).
18. Muljo, S. A. & Schlissel, M. S. A small molecule Abl kinase inhibitor induces differentiation of Abelson virus-transformed pre-B cell lines. Nature Immunol. 4, 31-37 (2003).
19. Liang, H. E. et al. The "dispensable" portion of RAG2 is necessary for efficient V-to-DJ rearrangement during B and T cell development. Immunity 17, 639-651 (2002).
20. Lewis, S. M., Hesse, J. E., Mizuuchi, K. & Gellert, M. Novel strand exchanges in V(D)J recombination. Cell 55, 1099-1107 (1988).
21. Morzycka-Wroblewska, E., Lee, F. E. & Desiderio, S. V. Unusual immunoglobulin gene rearrangement leads to replacement of recombinational signal sequences. Science 242, 261-263 (1988).
22. Hickson, I. et al. Identification and characterization of a novel and specific inhibitor of the ataxia-telangiectasia mutated kinase ATM. Cancer Res. 64, 9152-9159 (2004).
23. Roth, D. B., Menetski, J. P., Nakajima, P. B., Bosma, M. J. & Gellert, M. V(D)J recombination: broken DNA molecules with covalently sealed (hairpin) coding ends in scid mouse thymocytes. Cell 70, 983-991 (1992).
24. Franco, S. et al. H2AX prevents DNA breaks from progressing to chromosome breaks and translocations. Mol. Cell 21, 201-214 (2006).
25. Agrawal, A. & Schatz, D. G. RAG1 and RAG2 form a stable postcleavage synaptic complex with DNA containing signal ends in V(D)J recombination. Cell 89, 43-53 (1997).
26. Hiom, K. & Gellert, M. Assembly of a 12/23 paired signal complex: a critical control point in V(D)J recombination. Mol. Cell 1, 1011-1019 (1998).
27. Riballo, E. et al. A pathway of double-strand break rejoining dependent upon ATM, Artemis, and proteins locating to γ-H2AX foci. Mol. Cell 16, 715-724 (2004).
28. Sekiguchi, J. A., Whitlow, S. & Alt, F. W. Increased accumulation of hybrid V(D)J joins in cells expressing truncated versus full-length RAGs. Mol. Cell 8, 1383-1390 (2001).
29. Mills, K. D., Ferguson, D. O. & Alt, F. W. The role of DNA breaks in genomic instability and tumorigenesis. Immunol. Rev. 194, 77-95 (2003).