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Early events of B cell activation after B cell receptor (BCR) triggering have been well characterized. However, little is known about the steady state of the BCR on the cell surface. Here, we simultaneously visualize single BCR particles and components of the membrane skeleton. We show that an ezrin- and actin-defined network influenced steady-state BCR diffusion by creating boundaries that restrict BCR diffusion. We identified the intracellular domain of Igbeta as important in mediating this restriction in diffusion. Importantly, alteration of this network was sufficient to induce robust intracellular signaling and concomitant increase in BCR mobility. Moreover, by using B cells deficient in key signaling molecules, we show that this signaling was most probably initiated by the BCR. Thus, our results suggest the membrane skeleton plays a crucial function in controlling BCR dynamics and thereby signaling, in a way that could be important for understanding tonic signaling necessary for B cell development and survival.

Original publication

DOI

10.1016/j.immuni.2009.12.005

Type

Journal article

Journal

Immunity

Publication Date

26/02/2010

Volume

32

Pages

187 - 199

Keywords

Actins, Animals, Antigens, CD79, B-Lymphocytes, Bridged Bicyclo Compounds, Heterocyclic, Cell Line, Tumor, Cell Membrane, Cytoskeletal Proteins, Cytoskeleton, Immunologic Capping, Mice, Mice, Inbred C57BL, Mice, Knockout, Microscopy, Fluorescence, Protein Binding, Protein Engineering, Protein Structure, Tertiary, Signal Transduction, Thiazolidines