AID is required for germinal center-derived lymphomagenesis

Nature Genetics

Volumn 40, Issue 1, 2008, Pages 108-112

  Pasqualucci, Laura ^a   Bhagat, Govind ^a   Jankovic, Mila ^b   Compagno, Mara ^a   Smith, Paula ^a   Muramatsu, Masamichi ^c   Honjo, Tasuku ^d   Morse III, Herbert C ^e   Nussenzweig, Michel C ^b   Dalla Favera, Riccardo ^a  

^a Och Spine at New York Presbyterian Hospitals   (United States)

^b ROCKEFELLER UNIVERSITY   (United States)

^c KANAZAWA UNIVERSITY   (Japan)

^d KYOTO UNIVERSITY   (Japan)

^e NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ACTIVATION INDUCED CYTIDINE DEAMINASE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; B CELL LYMPHOMA; CARCINOGENESIS; CHROMOSOME TRANSLOCATION; CONTROLLED STUDY; ENZYME DEFICIENCY; GERMINAL CENTER; LYMPHOMA; MOUSE; NONHODGKIN LYMPHOMA; NONHUMAN; ONCOGENE MYC; PATHOGENESIS; PRIORITY JOURNAL;

ANIMALS; CELL TRANSFORMATION, NEOPLASTIC; CYTIDINE DEAMINASE; FEMALE; GERMINAL CENTER; LYMPHOMA, B-CELL; MALE; MICE; MICE, INBRED C57BL;

MUS;

EID: 37549068541     PISSN: 10614036     EISSN: 15461718     Source Type: Journal    
DOI: 10.1038/ng.2007.35     Document Type: Article

References (30)

1. Rajewsky, K. Clonal selection and learning in the antibody system. Nature 381, 751-758 (1996).
2. Ramiro, A.R. et al. AID is required for c-myc/IgH chromosome translocations in vivo. Cell 118, 431-438 (2004).
3. Pasqualucci, L. et al. Hypermutation of multiple proto-oncogenes in B cell diffuse large-cell lymphomas. Nature 412, 341-346 (2001).
4. Küppers, R. & Dalla-Favera, R. Mechanisms of chromosomal translocation in B cell lymphoma. Oncogene 20, 5580-5594 (2001).
5. Kovalchuk, A.L. et al. Burkitt lymphoma in the mouse. J. Exp. Med. 192, 1183-1190 (2000).
6. Cattoretti, G. et al. Deregulated BCL6 expression recapitulates the pathogenesis of human diffuse large B cell lymphomas in mice. Cancer Cell 7, 445-455 (2005).
7. 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).
8. 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).
9. Shaffer, A.L., Rosenwald, A. & Staudt, L.M. Lymphoid malignancies: the dark side of B cell differentiation. Nat. Rev. Immunol. 2, 920-932 (2002).
10. Dalla-Favera, R. & Pasqualucci, L. Molecular genetics of lymphoma. in Non-Hodgkin's Lymphoma (eds. Mauch, M.P., Armitage, J.O., Coiffier, B., Dalla-Favera, R. & Harris, N.) 825-843 (Lippincot Williams & Wilkins, Philadelphia, 2004).
11. Muramatsu, M. et al. Specific expression of activation-induced cytidine deaminase (AID), a novel member of the RNA-editing deaminase family in germinal center B cells. J. Biol. Chem. 274, 18470-18476 (1999).
12. Pasqualucci, L. et al. Expression of the AID protein in normal and neoplastic B cells. Blood 104, 3318-3325 (2004).
13. Petersen-Mahrt, S.K., Harris, R.S. & Neuberger, M.S. AID mutates E. coli suggesting a DNA deamination mechanism for antibody diversification. Nature 418, 99-103 (2002).
14. 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).
15. Chaudhuri, J. et al. Transcription-targeted DNA deamination by the AID antibody diversification enzyme. Nature 422, 726-730 (2003).
16. Di Noia, J. & Neuberger, M.S. Altering the pathway of immunoglobulin hypermutation by inhibiting uracil-DNA glycosylase. Nature 419, 43-48 (2002).
17. 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).
18. 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).
19. Ramiro, A.R. et al. Role of genomic instability and p53 in AID-induced c-Myc-Igh translocations. Nature 440, 105-109 (2006).
20. Franco, S. et al. H2AX prevents DNA breaks from progressing to chromosome breaks and translocations. Mol. Cell 21, 201-214 (2006).
21. Mollejo, M. et al. Nodal and splenic marginal zone B cell lymphomas. Hematol. Oncol. 23, 108-118 (2005).
22. Nagaoka, H., Muramatsu, M., Yamamura, N., Kinoshita, K. & Honjo, T. Activation-induced deaminase (AID)-directed hypermutation in the immunoglobulin Sμ region: implication of AID involvement in a common step of class switch recombination and somatic hypermutation. J. Exp. Med. 195, 529-534 (2002).
23. 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).
24. Phan, R.T. & Dalla-Favera, R. The BCL6 proto-oncogene suppresses p53 expression in germinal-centre B cells. Nature 432, 635-639 (2004).
25. Phan, R.T., Saito, M., Basso, K., Niu, H. & Dalla-Favera, R. BCL6 interacts with the transcription factor Miz-1 to suppress the cyclin-dependent kinase inhibitor p21 and cell cycle arrest in germinal center B cells. Nat. Immunol. 6, 1054-1060 (2005).
26. Ranuncolo, S.M. et al. Bcl-6 mediates the germinal center B cell phenotype and lymphomagenesis through transcriptional repression of the DNA-damage sensor ATR. Nat. Immunol. 8, 705-714 (2007).
27. Kotani, A. et al. Activation-induced cytidine deaminase (AID) promotes B cell lymphomagenesis in Eμ-cMyc transgenic mice. Proc. Natl. Acad. Sci. USA 104, 1616-1620 (2007).
28. Lenz, G. et al. Aberrant immunoglobulin class switch recombination and switch translocations in activated B cell-like diffuse large B cell lymphoma. J. Exp. Med. 204, 633-643 (2007).
29. 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).
30. Klein, U. et al. Gene expression profiling of B cell chronic lymphocytic leukemia reveals a homogeneous phenotype related to memory B cells. J. Exp. Med. 194, 1625-1638 (2001).