The Journal of Experimental Medicine
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Published 7 January 2002. doi:10.1084/jem.20011524
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© Rockefeller University Press, 0022-1007/2002/1/143/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 1, January 7, 2002 143-149

Brief Definitive Report

The B Lymphocyte Adaptor Molecule of 32 kD (Bam32) Regulates B Cell Antigen Receptor Signaling and Cell Survival

Hiroaki Niiro1, Akito Maeda3, Tomohiro Kurosaki3 and Edward A. Clark1,2

1 Department of Microbiology, University of Washington, Seattle, WA 98195
2 Department of Immunology, University of Washington, Seattle, WA 98195
3 Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570-8506, Japan

Address correspondence to Dr. Edward A. Clark, Department of Microbiology, Box 357242, University of Washington, Seattle, WA 98195. Phone: 206-543-8706; Fax: 206-685-0305; E-mail: eclark{at}bart.rprc.washington.edu

The B lymphocyte–associated adaptor protein 32 kD in size (Bam32) is expressed at high levels in germinal center (GC) B cells. It has an NH2-terminal src homology 2 (SH2) domain which binds phospholipase C (PLC){gamma}2, and a COOH-terminal pleckstrin homology (PH) domain. Thus, Bam32 may function to integrate protein tyrosine kinase (PTK) and phosphatidylinositol 3-kinase (PI3K) signaling pathways in B cells. To further define the role Bam32 plays in B cells, we generated Bam32-deficient DT40 cells. These Bam32-/- cells exhibited lower levels of B cell antigen receptor (BCR)-induced calcium mobilization with modest decreases in tyrosine phosphorylation of phospholipase C (PLC){gamma}2. Moreover, BCR-induced activation of extracellular signal-regulated kinase (ERK), c-jun NH2-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) pathways was impaired in Bam32-/- cells but not the activation of Akt-related pathways. Activation of downstream transcription factors such as nuclear factor of activated T cells (NF-AT) and nuclear factor of {kappa} binding (NF-{kappa}B) was also impaired in Bam32-/- cells. Furthermore, Bam32-/- cells were more susceptible to BCR-induced death. Taken together, these findings suggest that Bam32 functions to regulate BCR-induced signaling and cell survival most likely in germinal centers.

Key Words: adaptor protein • cell death • germinal center • PH domain • signal transduction


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