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J. Exp. Med.,
Volume 189, Number 1, January 4, 1999 123-129
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From the * Howard Hughes Medical Institute, Boston, Massachusetts 02115; To elucidate the intracellular pathways that mediate early B cell development, we directed expression of activated Ras to the B cell lineage in the context of the recombination-activating gene 1 (RAG1)-deficient background (referred to as Ras-RAG). Similar to the effects of an
immunoglobulin (Ig) µ heavy chain (HC) transgene, activated Ras caused progression of
RAG1-deficient progenitor (pro)-B cells to cells that shared many characteristics with precursor (pre)-B cells, including downregulation of surface CD43 expression plus expression of
The Children's
Hospital, Boston, Massachusetts 02115; the § Center for Blood Research and the
Department of
Genetics, Harvard Medical School, Boston, Massachusetts 02115; and the ¶ Infectious Disease Unit,
Massachusetts General Hospital, Boston, Massachusetts 02114
5,
RAG2, and germline
locus transcripts. However, these Ras-RAG pre-B cells also upregulated surface markers characteristic of more mature B cell stages and populated peripheral lymphoid tissues, with an overall phenotype reminiscent of B lineage cells generated in a RAG-
deficient background as a result of expression of an Ig µ HC together with a Bcl-2 transgene.
Taken together, these findings suggest that activated Ras signaling in pro-B cells induces developmental progression by activating both differentiation and survival signals.
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