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J. Biol. Chem., Vol. 269, Issue 44, 27365-27371, Nov, 1994
J Cheng, AA Guffanti and TA Krulwich
The chromosomal tetB(L) gene of Bacillus subtilis encodes a transporter
that catalyzes Na+/H+ antiport even more actively than tetracycline/H+
antiport, as shown by assays of membrane antiporter activity upon
transformation of Na+/H+ antiporter-deficient Escherichia coli with the
cloned gene; the transformation results in a substantial increase in Na+
resistance as well as detectable resistance to low tetracycline
concentrations. Transpositional disruption of the chromosomal tetB(L) locus
of B. subtilis led to reduced rates of electrogenic Na+ efflux and revealed
a physiological role for this locus in Na+ resistance and Na(+)-dependent
pH homeostasis at pH 8.5. The mutant phenotype was reversed by
transformation with a plasmid expressing the cloned tetB(L) gene.
Energy-dependent tetracycline efflux rates in the wild type were greater
than in the transposition mutant but were not sufficient to confer
resistance to the antibiotic. TetB(L) is also inferred to have a modest
capacity for K+ efflux, since the transposition mutant is slightly impaired
in K(+)-dependent pH homeostasis at pH 8.5 and grew better than the wild
type at pH 7 on limiting K+ concentrations.
The chromosomal tetracycline resistance locus of Bacillus subtilis encodes a Na+/H+ antiporter that is physiologically important at elevated pH
Department of Biochemistry, Mount Sinai School of Medicine of CUNY, New York 10029.
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