The Journal of Experimental Medicine
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Published 5 May 2003. doi:10.1084/jem.20022112
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© Rockefeller University Press, 0022-1007/2003/5/1221 $5.00
The Journal of Experimental Medicine, Volume 197, Number 9, 1221-1227

Brief Definitive Report

Regulation of Fyn Through Translocation of Activated Lck into Lipid Rafts

Dominik Filipp1, Jenny Zhang1, Bernadine L. Leung1, Andrey Shaw2, Steven D. Levin3, André Veillette4 and Michael Julius1

1 Sunnybrook and Women's College Health Sciences Centre, Department of Immunology, University of Toronto, Toronto, Ontario M4N 3M5, Canada
2 Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110
3 Department of Immunology, University of Washington, Seattle, WA 98195
4 Laboratory of Molecular Oncology, IRCM, and the Departments of Biochemistry, Medicine, and Microbiology and Immunology, McGill University, Montréal, Quebec H2W 1R7, Canada

Address correspondence to Michael Julius, Sunnybrook and Women's College Health Sciences Centre, Room A3 33, 2075 Bayview Ave., Toronto, Ontario M4N 3M5, Canada. Phone: 416-480-4650; Fax: 416-480-4351; E-mail: michael.julius{at}utoronto.ca

Whether or how the activation of Lck and Fyn during T cell receptor (TCR) signaling is coordinated, and their delivery of function integrated, is unknown. Here we show that lipid rafts function to segregate Lck and Fyn in T cells before activation. Coaggregation of TCR and CD4 leads to Lck activation within seconds outside lipid rafts, followed by its translocation into lipid rafts and the activation of colocalized Fyn. Genetic evidence demonstrates that Fyn activation is strictly dependent on receptor-induced translocation of Lck. These results characterize the interdependence of Lck and Fyn function and establish the spatial and temporal distinctions of their roles in the cellular activation process.

Key Words: Src kinases • T cell • lipid rafts • colocalization • sequential activation


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