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and Ig-
1
* Biologie III, University of Freiburg and Max-Planck-Institute for Immunobiology, Freiburg, Germany;
Department of Immunology, National Jewish Medical and Research Center, Denver, CO 80206;
Howard Hughes Medical Institute, Rockefeller University, New York, NY 10021
Ig-
and Ig-
mediate surface expression and signaling of
diverse B cell receptor complexes on precursor, immature, and mature B
cells. Their expression begins before that of the Ig chains in early
progenitor B cells. In this study, we describe the generation of
Ig--deficient mice and their comparative analysis to mice deficient
for Ig-, the membrane-IgM, and recombination-activating gene
2 to determine the requirement of Ig- and Ig- in survival
and differentiation of pro-B cells. We find that in the absence of
Ig-, B cell development does not progress beyond the progenitor
stage, similar to what is observed in humans lacking this molecule.
However, neither in Ig-- nor in Ig--deficient mice are pro-B
cells impaired in V(D)J recombination, in the expression of
intracellular Ig µ-chains, or in surviving in the bone marrow
microenvironment. Finally, Ig- and Ig- are not redundant in their
putative function, as pro-B cells from Ig- and Ig-
double-deficient mice are similar to those from single-deficient
animals in every aspect analyzed.
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