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Am J Physiol Cell Physiol 275: C1291-C1299, 1998;
0363-6143/98 $5.00
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Vol. 275, Issue 5, C1291-C1299, November 1998

Tyrosine kinase-deficient Wv c-kit induces mast cell adhesion and chemotaxis

Jaroslaw Dastych1, Dennis Taub2, Mary C. Hardison3, and Dean D. Metcalfe3

1 Department of Biogenic Amines, Polish Academy of Sciences, 90-950 Lodz, Poland; 2 Clinical Services Program, Sciences Applications International Corporation, Frederick Cancer Research and Development Center, National Cancer Institute, Frederick, 21702; and 3 Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892

W/Wv mice are deficient in tissue mast cells, and mast cells cultured from these mice do not proliferate in response to the c-kit ligand, stem cell factor (SCF). In this paper, we report that mouse bone marrow cultured mast cells derived from W/Wv mice do adhere to fibronectin in the presence of SCF and exhibit chemotaxis to SCF, and we explore this model for the understanding of c-kit-mediated signaling pathways. Both in vitro and in vivo (in intact cells) phosphorylation experiments demonstrated a low residual level of W/Wv c-kit protein phosphorylation. SCF-induced responses in W/Wv mast cells were abolished by the tyrosine kinase inhibitor herbimycin A and by the phospatidylinositol 3-kinase (PI 3-kinase) inhibitor wortmannin but were not affected by protein kinase C inhibitors. These observations are consistent with the conclusions that Wv c-kit initiates a signaling process that is PI 3-kinase dependent and that mutated Wv c-kit retains the ability to initiate mast cell adhesion and migration.

stem cell factor; W/Wv mice; phosphatidylinositol 3-kinase-dependent adhesion; fibronectin


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