53BP1 links DNA damage-response pathways to immunoglobulin heavy chain class-switch recombination (original) (raw)

• van Gent, D.C., Hoeijmakers, J.H. & Kanaar, R. Chromosomal stability and the DNA double-stranded break connection. Nat. Rev. Genet. 2, 196–206 (2001).
  Article CAS Google Scholar
• 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).
  Article CAS Google Scholar
• Jackson, S.P. Sensing and repairing DNA double-strand breaks. Carcinogenesis 23, 687–696 (2002).
  Article CAS Google Scholar
• Bassing, C.H., Swat, W. & Alt, F.W. The mechanism and regulation of chromosomal V(D)J recombination. Cell 109, S45–S55 (2002).
  Article CAS Google Scholar
• Manis, J.P., Tian, M. & Alt, F.W. Mechanism and control of class-switch recombination. Trends Immunol. 23, 31–39 (2002).
  Article CAS Google Scholar
• Jung, D. & Alt, F.W. Unraveling V(D)J recombination: Insights into gene regulation. Cell 116, 299–311 (2004).
  Article CAS Google Scholar
• Storb, U. & Stavnezer, J. Immunoglobulin genes: generating diversity with AID and UNG. Curr. Biol. 12, 725–727 (2002).
  Article Google Scholar
• Papavasiliou, F.N. & Schatz, D.G. Somatic hypermutation of immunoglobulin genes: merging mechanisms for genetic diversity. Cell 109, S35–44 (2002).
  Article CAS Google Scholar
• Revy, P. et al. Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the hyper-IgM syndrome (HIGM2). Cell 102, 565–575 (2000).
  Article CAS Google Scholar
• Muramatsu, M. et al. Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme. Cell 102, 553–563 (2000).
  Article CAS Google Scholar
• Chaudhuri, J. et al. Transcription-targeted DNA deamination by the AID antibody diversification enzyme. Nature 422, 726–730 (2003).
  Article CAS Google Scholar
• Ramiro, A.R., Stavropoulos, P., Jankovic, M. & Nussenzweig, M.C. Transcription enhances AID-mediated cytidine deamination by exposing single-stranded DNA on the nontemplate strand. Nat. Immunol. 4, 452–456 (2003).
  Article CAS Google Scholar
• Bransteitter, R., Pham, P., Scharff, M.D. & Goodman, M.F. Activation-induced cytidine deaminase deaminates deoxycytidine on single-stranded DNA but requires the action of RNase. Proc. Natl. Acad. Sci. USA 100, 4102–4107 (2003).
  Article CAS Google Scholar
• Dickerson, S.K., Market, E., Besmer, E. & Papavasiliou, F.N. AID mediates hypermutation by deaminating single stranded DNA. J. Exp. Med. 197, 1291–1296 (2003).
  Article CAS Google Scholar
• Neuberger, M.S., Harris, R.S., Di Noia, J. & Petersen-Mahrt, S.K. Immunity through DNA deamination. Trends Biochem. Sci. 28, 305–312 (2003).
  Article CAS Google Scholar
• Li, Z., Woo, C.J., Iglesias-Ussel, M.D., Ronai, D. & Scharff, M.D. The generation of antibody diversity through somatic hypermutation and class switch recombination. Genes Dev. 18, 1–11 (2004).
  Article Google Scholar
• Chua, K.F., Alt, F.W. & Manis, J.P. The function of AID in somatic mutation and class switch recombination: upstream or downstream of DNA breaks. J. Exp. Med. 195, F37–41 (2002).
  Article CAS Google Scholar
• Reynaud, C.A., Aoufouchi, S., Faili, A. & Weill, J.C. What role for AID: mutator, or assembler of the immunoglobulin mutasome? Nat. Immunol. 4, 631–638 (2003).
  Article CAS Google Scholar
• Zhou, B.B. & Elledge, S.J. The DNA damage response: putting checkpoints in perspective. Nature 408, 433–439 (2000).
  Article CAS Google Scholar
• Abraham, R.T. Cell cycle checkpoint signaling through the ATM and ATR kinases. Genes Dev. 15, 2177–2196 (2001).
  Article CAS Google Scholar
• Xia, Z., Morales, J.C., Dunphy, W.G. & Carpenter, P.B. Negative cell cycle regulation and DNA damage-inducible phosphorylation of the BRCT protein 53BP1. J. Biol. Chem. 276, 2708–2718 (2001).
  Article CAS Google Scholar
• Schultz, L.B., Chehab, N.H., Malikzay, A. & Halazonetis, T.D. p53 binding protein 1 (53BP1) is an early participant in the cellular response to DNA double-strand breaks. J. Cell. Biol. 151, 1381–1390 (2000).
  Article CAS Google Scholar
• Anderson, L., Henderson, C. & Adachi, Y. Phosphorylation and rapid relocalization of 53BP1 to nuclear foci upon DNA damage. Mol. Cell. Biol. 21, 1719–1729 (2001).
  Article CAS Google Scholar
• Rappold, I., Iwabuchi, K., Date, T. & Chen, J. Tumor suppressor p53 binding protein 1 (53BP1) is involved in DNA damage-signaling pathways. J. Cell Biol. 153, 613–620 (2001).
  Article CAS Google Scholar
• Rogakou, E.P., Pilch, D.R., Orr, A.H., Ivanova, V.S. & Bonner, W.M. DNA double-stranded breaks induce histone H2AX phosphorylation on serine 139. J. Biol. Chem. 273, 5858–5868 (1998).
  Article CAS Google Scholar
• Morales, J.C. et al. Role for the BRCA1 C-terminal repeats (BRCT) protein 53BP1 in maintaining genomic stability. J. Biol. Chem. 278, 14971–14977 (2003).
  Article CAS Google Scholar
• Ward, I.M., Minn, K., van Deursen, J. & Chen, J. p53 Binding protein 53BP1 is required for DNA damage responses and tumor suppression in mice. Mol. Cell. Biol. 23, 2556–2563 (2003).
  Article CAS Google Scholar
• Stavnezer, J. Antibody class switching. Adv. Immunol. 61, 79–146 (1996).
  Article CAS Google Scholar
• Chu, C.C., Max, E.E. & Paul, W.E. DNA rearrangement can account for in vitro switching to IgG1. J. Exp. Med. 178, 1381–1390 (1993).
  Article CAS Google Scholar
• Lutzker, S. & Alt, F.W. Structure and expression of germ line immunoglobulin γ2b transcripts. Mol. Cell. Biol. 8, 1849–1852 (1988).
  Article CAS Google Scholar
• Yu, K. & Lieber, M.R. Nucleic acid structures and enzymes in the immunoglobulin class switch recombination mechanism. DNA Repair (Amst) 2, 1163–1174 (2003).
  Article CAS Google Scholar
• Hodgkin, P.D., Lee, J.H. & Lyons, A.B. B cell differentiation and isotype switching is related to division cycle number. J. Exp. Med. 184, 277–281 (1996).
  Article CAS Google Scholar
• Jolly, C.J., Klix, N. & Neuberger, M.S. Rapid methods for the analysis of immunoglobulin gene hypermutation: application to transgenic and gene targeted mice. Nucleic Acids Res. 25, 1913–1919 (1997).
  Article CAS Google Scholar
• Iwabuchi, K. et al. Potential role for 53BP1 in DNA end-joining repair through direct interaction with DNA. J. Biol. Chem. 278, 36487–36495 (2003).
  Article CAS Google Scholar
• Xu, Y. et al. Targeted disruption of ATM leads to growth retardation, chromosomal fragmentation during meiosis, immune defects, and thymic lymphoma. Genes Dev. 10, 2411–2422 (1996).
  Article CAS Google Scholar
• Manis, J.P., Dudley, D., Kaylor, L. & Alt, F.W. IgH class switch recombination to IgG1 in DNA-PKcs-deficient B cells. Immunity 16, 607–617 (2002).
  Article CAS Google Scholar
• Bosma, G.C. et al. DNA-dependent protein kinase activity is not required for immunoglobulin class switching. J. Exp. Med. 196, 1483–1495 (2002).
  Article CAS Google Scholar
• Cook, A.J. et al. Reduced switching in SCID B cells is associated with altered somatic mutation of recombined S regions. J. Immunol. 171, 6556–6564 (2003).
  Article CAS Google Scholar
• Fernandez-Capetillo, O. et al. DNA damage-induced G2-M checkpoint activation by histone H2AX and 53BP1. Nat. Cell Biol. 4, 993–997 (2002).
  Article CAS Google Scholar
• Wang, B., Matsuoka, S., Carpenter, P.B. & Elledge, S.J. 53BP1, a mediator of the DNA damage checkpoint. Science 298, 1435–1438 (2002).
  Article CAS Google Scholar
• DiTullio, R.A., Jr. et al. 53BP1 functions in an ATM-dependent checkpoint pathway that is constitutively activated in human cancer. Nat. Cell. Biol. 4, 998–1002 (2002).
  Article CAS Google Scholar
• Petersen, S. et al. AID is required to initiate Nbs1/γ-H2AX focus formation and mutations at sites of class switching. Nature 414, 660–665 (2001).
  Article CAS Google Scholar
• Bassing, C.H. et al. Increased ionizing radiation sensitivity and genomic instability in the absence of histone H2AX. Proc. Natl. Acad. Sci. USA 99, 8173–8178 (2002).
  Article CAS Google Scholar
• Reina-San-Martin, B. et al. H2AX is required for recombination between immunoglobulin switch regions but not for intra-switch region recombination or somatic hypermutation. J. Exp. Med. 197, 1767–1778 (2003).
  Article CAS Google Scholar
• Celeste, A. et al. Genomic instability in mice lacking histone H2AX. Science 296, 922–927 (2002).
  Article CAS Google Scholar
• Bassing, C.H. & Alt, F.W. H2AX may function as an anchor to hold broken chromosomal DNA ends in close proximity. Cell Cycle 3, e119–e123 (2004).
  Article Google Scholar
• Li, Y.S., Hayakawa, K. & Hardy, R.R. The regulated expression of B lineage associated genes during B cell differentiation in bone marrow and fetal liver. J. Exp. Med. 178, 951–960 (1993).
  Article CAS Google Scholar
• Ehrenstein, M.R. & Neuberger, M.S. Deficiency in Msh2 affects the efficiency and local sequence specificity of immunoglobulin class-switch recombination: parallels with somatic hypermutation. EMBO J. 18, 3484–3490 (1999).
  Article CAS Google Scholar
• Casola, S. et al. B cell receptor signal strength determines B cell fate. Nat. Immunol. 5, 317–327 (2004).
  Article CAS Google Scholar