REGULATION OF KDP OPERON EXPRESSION IN ESCHERICHIA-COLI - EVIDENCE AGAINST TURGOR AS SIGNAL FOR TRANSCRIPTIONAL CONTROL

Kdp, an inducible high-affinity K+ transporter in Escherichia coli, is encoded by genes of the kdpABC operon, and its expression is regulate d by the products of kdpD and kdpE. Loss of cell turgor has been propo sed to be the signal which induces kdp expression (L. A. Laimins, D. B . Rhoads, and W. Epstein, Proc. Natl. Acad. Sci. USA 78:464-468, 1981) . We reexamined kdp expression during steady-state growth under a vari ety of conditions and were able to confirm earlier observations which had indicated that it is primarily affected by the concentration of K in the medium and by mutations in genes encoding various K+ transport ers in E. coli. Changes in pH of the culture also altered kdp expressi on. In all of these cases, an increase in [K+] of the medium repressed the operon. Several ionic solutes induced steady-state kdp expression (but to differing extents), whereas nonionic solutes had no effect, i ndicating that kdp expression is not determined by osmolarity of the g rowth medium. kdp expression during steady-state growth was shown also to be unaffected by the accumulation of other intracellular compatibl e solutes such as trehalose or glycine betaine, which would be expecte d to restore cell turgor during growth in high-osmolarity media. Two m utants that are defective in perception of the signal regulating kdp w ere isolated, and the mutation in each of them was mapped to the kdpDE regulatory locus. Analysis of kdp expression in one of these mutants provided additional evidence against the turgor regulation model. On t he basis of these data, we discuss alternative candidates that might s erve as the signal for control of kdp operon transcription.