Transcrip-2 + tion of PmrA-activated genes is induced in low Mg in a process that requires the PhoP and PhoQ proteins , the PhoP-activated pmrD gene as well as the PmrA and PmrB proteins ( Kox et al. , 2000 ) .
The highly divergent PmrD protein is responsible for this phenotype as replacement of the E. coli pmrD gene by its Salmonella counterpart resulted in an E. coli strain that transcribed PmrA-activated genes and displayed poly-myxin B resistance under the same conditions as Salmonella .
This behavior is due to the highly divergent PmrD protein ( Figs. 6 and 7 ) , because replacement of the E. coli pmrD gene by the Salmonella pmrD gene endowed E. coli with the ability to transcribe the PmrA-activated pbgP gene and to exhibit resistance to polymyxin B in response to the low Mg2 signal ( Fig. 3 ) .