The Journal of Cell Biology, Vol 110, 1217-1226, Copyright © 1990 by The Rockefeller University Press

ARTICLES

The action of v-src on gap junctional permeability is modulated by pH

K Hyrc and B Rose
Department of Physiology and Biophysics, University of Miami School of Medicine, Florida 33101.

The product of the viral src gene (v-src) is the protein tyrosine kinase pp60v-src. Among the known consequences of pp60v-src activity is the reduction in permeability of gap junctions, an effect that is counteracted by the calcium antagonist TMB-8 (8-N,N-[diethylamino]octyl- 3,4,5-trimethoxybenzoate). We show here that a decrease in intracellular pH (pHi) also counteracts the v-src effect: junctional permeability of cells containing active v-src kinase rose with decreasing pHi in the range 7.15 to 6.75, whereas junctional permeability of cells containing inactive v-src kinase or no v-src at all was insensitive to pH in that range. Low pH also counteracted the known action of diacylglycerol on junction, but only when pp60v-src kinase was inactive. Immunoblots of whole-cell lysates using an antibody against phosphotyrosine show that phosphorylation on tyrosine of at least one cellular protein, specific for pp60v-src kinase activity, was reduced by low pH but not by TMB-8. These results suggest that TMB-8 does not inhibit v-src action on junctional permeability by interfering with tyrosine phosphorylation of a protein crucial for closure of gap junction channels, but that the inhibition by low pH may be via this mechanism.
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This article has been cited by other articles:

• Sater, A., Alderton, J., Steinhardt, R. (1994). An increase in intracellular pH during neural induction in Xenopus. Development 120: 433-442 [Abstract]  

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