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J. Exp. Med.,
Volume 189, Number 11, June 7, 1999 1685-1690
By
§
From the * Department of Biology, Boston College, Chestnut Hill, Massachusetts 02467; the B-1 lymphocytes represent a distinct B cell subset with characteristic features that include self-renewing capacity and unusual mitogenic responses. B-1 cells differ from conventional B cells in terms of the consequences of phorbol ester treatment: B-1 cells rapidly enter S phase in response to phorbol ester alone, whereas B-2 cells require a calcium ionophore in addition to
phorbol ester to trigger cell cycle progression. To address the mechanism underlying the varied
proliferative responses of B-1 and B-2 cells, we evaluated the expression and activity of the
G1 cell cycle regulator, cyclin D2, and its associated cyclin-dependent kinases (Cdks). Cyclin D2 expression was upregulated rapidly, within 2-4 h, in phorbol ester-stimulated B-1 cells, in
a manner dependent on intact transcription/translation, but was not increased in phorbol ester-
stimulated B-2 cells. Phorbol ester-stimulated cyclin D2 expression was accompanied by the
formation of cyclin D2-Cdk4, and, to a lesser extent, cyclin D2-Cdk6, complexes; cyclin D2-
containing complexes were found to be catalytically functional, in terms of their ability to
phosphorylate exogenous Rb in vitro and to specifically phosphorylate endogenous Rb on
serine780 in vivo. These results strongly suggest that the rapid induction of cyclin D2 by a normally nonmitogenic phorbol ester stimulus is responsible for B-1 cell progression through G1
phase. The ease and rapidity with which cyclin D2 responds in B-1 cells may contribute to the
proliferative features of this subset.
Department of Medicine, the § Department of Microbiology, and The Evans Memorial Department of
Clinical Research, Boston University Medical Center, Boston, Massachusetts 02118; and the ¶ Division of Cancer Biology, Danish Cancer Society, Copenhagen, Denmark DK-2100
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