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Originally published In Press as doi:10.1074/jbc.M003397200 on September 28, 2000

J. Biol. Chem., Vol. 276, Issue 2, 1041-1050, January 12, 2001
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Interaction between the Unphosphorylated Receptor with High Affinity for IgE and Lyn Kinase*

Becky M. VonakisDagger §, Hana Haleem-SmithDagger , Peter Benjamin, and Henry Metzger||

From the Section on Chemical Immunology, Arthritis and Rheumatism Branch, NIAMS, National Institutes of Health, Bethesda, Maryland 20892-1820

Chinese hamster ovary fibroblasts previously transfected with the high affinity receptor for IgE (Fcepsilon RI) were further transfected with the alpha  subunit of the receptor for interleukin 2 (Tac) or with chimeric constructs in which the cytoplasmic domain of Tac was replaced with the C-terminal cytoplasmic domain of either the beta  subunit or the gamma  subunit of Fcepsilon RI. Whereas native Tac failed to affect the aggregation-induced phosphorylation of Fcepsilon RI, both chimeric constructs substantially inhibited this reaction. Alternatively, the Fcepsilon RI-bearing fibroblasts were transfected with two chimeric constructs in which the cytoplasmic domain of Tac was replaced with a modified short form of Lyn kinase. The Lyn in both of the chimeric constructs had been mutated to remove the sites that are normally myristoylated and palmitoylated, respectively; one of the constructs had in addition been altered to be catalytically inactive. The catalytically active construct enhanced, and the inactive construct inhibited, aggregation-induced phosphorylation of the receptors. All of the chimeric constructs were largely distributed outside the detergent resistant microdomains, and whereas aggregation caused them to move to the domains in part, their aggregation was neither necessary nor enhanced their effects. These results and others indicate that the receptor and Lyn interact through protein-protein interactions that neither are dependent upon either the post-translational modification of the kinase with lipid moieties nor result exclusively from their co-localization in specialized membrane domains.

* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger These authors contributed equally to this work.

§ Present address: Allergy and Clinical Immunology Division, John Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Baltimore, MD 21224-6108.

Present address: 16 Franklin Woods Dr., Somers, CT 06071.

|| To whom correspondence should be addressed: Bldg. 10, Rm. 9N-228, 10 Center Dr., MSC-1820, NIAMS, NIH, Bethesda, MD 20892-1820. Tel.: 301-435-6126; Fax: 301-402-0012; E-mail: metzgerh@exchange.nih.gov.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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