The Journal of Experimental Medicine
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Published online 8 December 2003 doi:10.1084/jem.20030729
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© Rockefeller University Press, 0022-1007/2003/12/1863 $5.00
The Journal of Experimental Medicine, Volume 198, Number 12, 1863-1873

Mimicry of Pre–B Cell Receptor Signaling by Activation of the Tyrosine Kinase Blk

Theresa Tretter, Ashley E. Ross, Dominic I. Dordai and Stephen Desiderio

Department of Molecular Biology and Genetics, Howard Hughes Medical Institute and Program in Immunology, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205

Address correspondence to Stephen Desiderio, Department of Molecular Biology and Genetics, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, PCTB 701, Baltimore, MD 21205. Phone: (410) 955-4735; Fax: (410) 955-9124; email: sdesider{at}jhmi.edu

During B lymphoid ontogeny, assembly of the pre–B cell receptor (BCR) is a principal developmental checkpoint at which several Src-related kinases may play redundant roles. Here the Src-related kinase Blk is shown to effect functions associated with the pre-BCR. B lymphoid expression of an active Blk mutant caused proliferation of B progenitor cells and enhanced responsiveness of these cells to interleukin 7. In mice lacking a functional pre-BCR, active Blk supported maturation beyond the pro–B cell stage, suppressed VH to DJH rearrangement, relieved selection for productive heavy chain rearrangement, and stimulated {kappa} rearrangement. These alterations were accompanied by tyrosine phosphorylation of immunoglobulin ß and Syk, as well as changes in gene expression consistent with developmental maturation. Thus, sustained activation of Blk induces responses normally associated with the pre-BCR.

Key Words: B cell development • signal transduction • allelic exclusion • V(D)J recombination • Src kinases

T. Tretter and A.E. Ross contributed equally to this work.

The online version of this article contains supplemental material.

Abbreviations used in this paper: BCR, B cell receptor; NF, nuclear factor.


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