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Published online before print November 11, 2003

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(Journal of Leukocyte Biology. 2003;74:1139-1143.)
© 2003 by Society for Leukocyte Biology

Cyclin D2 controls B cell progenitor numbers

Azim Mohamedali^*, Inês Soeiro, Nicholas C. Lea^*, Janet Glassford, Lolita Banerji, Ghulam J. Mufti^*, Eric W.-F. Lam and N. Shaun B. Thomas^*,1

^* Department of Haematological Medicine, Leukaemia Sciences, Guy’s, King’s, St. Thomas’ School of Medicine, Rayne Institute, London, United Kingdom; and
Cancer Research–UK Labs and Section of Cancer Cell Biology, Imperial College School of Medicine at Hammersmith Hospital, London, United Kingdom

¹Correspondence: Department of Haematological Medicine, Leukaemia Sciences, Guy’s, King’s, St. Thomas’ School of Medicine, Rayne Institute, 123 Coldharbour Lane, London SE5 9RS, UK. E-mail: nicholas.s.thomas{at}kcl.ac.uk

Cyclin D2 affects B cell proliferation and differentiation in vivo. It is rate-limiting for B cell receptor (BCR)-dependent proliferation of B cells, and cyclin D2^-/- mice lack CD5+(B1) B lymphocytes. We show here that the bone marrow (BM) of cyclin D2^-/- mice contains half the numbers of Sca1+B220+ B cell progenitors but normal levels of Sca1+ progenitor cells of other lineages. In addition, clonal analysis of BM from the cyclin D2^-/- and cyclin D2^+/+ mice confirmed that there were fewer B cell progenitors (B220+) in the cyclin D2^-/- mice. In addition, the colonies from cyclin D2^-/- mice were less mature (CD19^lo) than those from cyclin D2^+/+ mice (CD19^Hi). The number of mature B2 B cells in vivo is the same in cyclin D2^-/- and cyclin D2^+/+ animals. Lack of cyclin D2 protein may be compensated by cyclin D3, as cyclin-dependent kinase (cdk)6 coimmunoprecipitates with cyclin D3 but not cyclin D1 from BM mononuclear cells of cyclin D2^-/- mice. It is active, as endogenous retinoblastoma protein is phosphorylated at the cdk6/4-cyclin D-specific sites, S^807/811. We conclude that cyclin D2 is rate-limiting for the production of B lymphoid progenitor cells whose proliferation does not depend on BCR signaling.

Key Words: mouse • bone marrow • Sca1+ • B lymphocytes • cellular proliferation

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