DUAL REGULATION OF INAA BY THE MULTIPLE ANTIBIOTIC-RESISTANCE (MAR) AND SUPEROXIDE (SOXRS) STRESS-RESPONSE SYSTEMS OF ESCHERICHIA-COLI

The roles of the marRAB (multiple antibiotic resistance) operon and soxRS (superoxide response) genes in the regulation of inaA, an unlinked weak-acid-inducible gene, were studied. inaA expression was estimated from the beta-galactosidase activity of a chromosomal inaA1::lacZ transcriptional fusion. marR mutations that elevate marRAB transcription and engender multiple antibiotic resistance elevated inaA expression by 10- to 20-fold over that of the wild-type. Similarly, one class of inaA constitutive mutants that mapped to the mar region were multiply antibiotic resistant. Overexpression of marA alone on a multicopy plasmid caused high constitutive expression of inaA in a strain with an extensive (39-kbp) marRAB deletion. Salicylate, an inducer of marRAB and of an unidentified mar-independent antibiotic resistance system, induced inaA by 6-fold. A portion of this induction was: also mar independent. Two soxRS constitutive mutants that were tested showed elevated levels of inaA. Paraquat, an inducer of the soxRS system, elevated inaA expression by 6- to 9-fold. This induction was soxRS dependent and hot mar dependent, whereas induction of inaA by salicylate was not dependent on soxRS. Paraquat induced resistance to norfloxacin in the mar-deleted strain but not in a soxRS-deleted strain. Thus, induction of multiple antibiotic resistance and inaA by salicylate occurs via mar and an unidentified pathway, while induction by paraquat occurs via soxRS.