Article abstract


Nature Immunology 8, 705 - 714 (2007)
Published online: 10 June 2007 | doi:10.1038/ni1478

Bcl-6 mediates the germinal center B cell phenotype and lymphomagenesis through transcriptional repression of the DNA-damage sensor ATR

Stella Maris Ranuncolo1, Jose M Polo1, Jamil Dierov2, Michael Singer3, Tracy Kuo4, John Greally5, Roland Green3, Martin Carroll2 & Ari Melnick1


Antibody specificity and diversity is generated in B cells during germinal center maturation through clonal expansion while they undergo class-switch recombination and somatic hypermutation. Here we demonstrate that the transcriptional repressor Bcl-6 mediates this phenotype by directly repressing ATR in centroblasts and lymphoma cells. ATR is critical in replication and DNA damage–sensing checkpoints. Bcl-6 allowed B cells to evade ATR-mediated checkpoints and attenuated the response of the B cells to exogenous DNA damage. Repression of ATR was necessary and sufficient for those Bcl-6 activities. CD40 signaling 'rescued' B cells from those effects by disrupting the Bcl-6 transcription-repression complex on the promoter of the gene encoding ATR. Our data demonstrate a transcriptional regulatory loop whereby Bcl-6 mediates the centroblast phenotype through transient silencing of ATR.

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  1. Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
  2. Hematology-Oncology Division, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
  3. NimbleGen Systems, Madison, Wisconsin 53711, USA.
  4. Department of Molecular and Cell Biology, Division of Immunology, University of California, Berkeley, California 94720, USA.
  5. Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

Correspondence to: Martin Carroll2 e-mail: carroll2@mail.med.upenn.edu

Correspondence to: Ari Melnick1 e-mail: amelnick@aecom.yu.edu


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