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J Biol Chem, Vol. 275, Issue 5, 3479-3484, February 4, 2000

Cyclin D3 Compensates for Loss of Cyclin D2 in Mouse B-lymphocytes Activated via the Antigen Receptor and CD40*

Eric W.-F. Lamabcd, Janet Glassfordabd, Lolita Banerjia, N. Shaun B. Thomasef, Piotr Sicinskig, and Gerry G. B. Klaush

From the a Ludwig Institute for Cancer Research and Section of Virology and Cell Biology, Imperial College School of Medicine at St Mary's, Norfolk Place, London W2 1PG, the e Department of Haematology, Royal Free and University College Medical School, 98 Chenies Mews, London WC1E 6HX, United Kingdom, the g Dana-Farber Cancer Institute and Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, and the h Division of Cellular Immunology, National Institute for Medical Research, Mill Hill, London NW7 1AA, United Kingdom

Cyclin D2 is the only D-type cyclin expressed in mature mouse B-lymphocytes, and its expression is associated with retinoblastoma protein (pRB) and pRB-related protein phosphorylation and induction of E2F activity, as B-cells enter the cell cycle following stimulation via surface IgM and/or CD40. Cyclin D-dependent kinase activity is required for cell proliferation, yet cyclin D2-/- mice have normal levels of mature B-lymphocytes. Here we show that B-lymphocytes from cyclin D2-/- mice can proliferate in response to anti-IgM and anti-CD40, but the time taken to enter S-phase is longer than for the corresponding cyclin D2+/+ cells. This is due to the compensatory induction of cyclin D3, but not cyclin D1, which causes pRb phosphorylation on CDK4-specific sites. This is the first demonstration that loss of a D-type cyclin causes specific expression and functional compensation by another member of the family in vivo and provides a rationale for the presence of mature B-lymphocytes in cyclin D2-/- mice.

* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

b Both authors contributed equally to this study and should be considered joint first authors.

c To whom correspondence should be addressed: Ludwig Institute for Cancer Research and Section of Virology and Cell Biology, Imperial College School of Medicine at St. Mary's Campus, Norfolk Place, London W2 1PG, UK. Tel.: 44-171-724-5522 (ext. 213); Fax: 44-171-724-8586; E-mail: eric.lam@ic.ac.uk.

d Supported by the Ludwig Institute for Cancer Research and the Leukemia Research Fund.

f Supported by the Kay Kendall Leukemia Trust. Current address: Dept. of Haematological Medicine, The Rayne Institute, 123 Cold Harbour Ln., London SE5 9NU, UK.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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