In the case of PmrA/B regulation , the response regulator PhoP activates pmrD .
We have investigated the transcriptional regulation and the interaction of the response regulator PhoP with the promoter regions of the PhoP-activated loci phoPQ , mgtA , slyB , pmrD , pcgL , phoN , pagC , and mgtCB .
However , the E. coli pmrD gene was induced in low Mg2 in a phoP-dependent manner , like other members of the E. coli PhoP regulon .
However , the E. coli pmrD gene was induced in low Mg2 in Fig. 5A , like other members of the E. coli PhoP regulon .
The mRNA lev - encoded products are produced in the correct els of the PhoP-activated mgtA , phoP , pmrD , locales , at the required amounts and for the ap - and mig-14 genes increased after the shift to low propriate extents of time .
As shown in Fig. 4C , this motif is also observed in a similar position and in the same orientation in a subset of PhoP-activated genes , including phoP , mgtA , pmrD , yrbL , slyB , and orgB ( 49 ) .
otes time-dependent resistance to polymyxin B MgtA prom The PhoP-activated pmrD and ugtL genes encode products mediating the chemical modification of negatively charged residues in the lipopolysaccharide ( LPS ) , thereby conferring resistance to the cationic peptide antibiotic polymyxin B ( Kox et al. , 2000 ; Shi et al. , 2004 ) .
A similar motif is found in the promoters of a subset of PhoP-activated genes , including steA , phoP , mgtA , pmrD , slyB , and orgB ( Fig. 6B ) .
In S. Typhimurium , the PhoPQ TCS indirectly activates the PmrAB TCS via PhoP-activated pmrD expression ( Kox et al. , 2000 ) .