Fig 4. ToxR wing mutants expressed from the toxR chromosomal locus are not preferentially defective for toxT activation.

A) Selected ToxR wing mutants representing each class of mutant were placed on the chromosome and assayed for transcriptional activation of toxT-lacZ and ompU-lacZ by β-galactosidase assay. Class I mutants were at least 2-fold more defective for toxT activation than ompU activation when expressed from a plasmid, but equally defective for activation of both promoters when endogenously expressed. Class II mutants are not defective for activation of either promoter, and maintained ≥90% activity even when mutated. Class III mutants are defective for activation of both promoters. * p<0.0045 using the Students’ T-test and a cut-off for significance at 0.05/11 according to the Bonferroni correction for multiple comparisons. B) The stability of each ToxR wing mutant was monitored by Western blot using anti-ToxR antibodies.