Previous work from our laboratory demonstrated that PhoP also regulates mig-14 .
We determined that a ugtL pmrA double mutant was as susceptible to polymyxin B as a phoP mutant ( Fig. 3C ) , which suggests that both types of lipid-A modifications may operate at the same time and argues against the participation of other PhoP-regulated genes in resistance to polymxyin B. Thus , the increased polymyxin B susceptibility reported for mutants defective in the PhoP-activated mig-14 , virK and somA genes may be characteristic of the SL1344 genetic background used in those studies ( Brodsky et al. , 2002 ; Detweiler et al. , 2003 ) because derivatives of the 14028s strain deleted for the mig-14 gene or harbouring a MudJ transposon insertion in the virK gene retained wild-type resistance to both polymxyin B and magainin 2 ( our unpublished results ) .
The PhoP-acti-vated mig-14 , mgtC , virK , and pagC promoters of Salmonella do not harbor a typical PhoP box in place of the 35 region , as found in archetypal PhoP-regulated promoters such as the mgtA promoter ( 13 ) .
mRNA levels of other PhoP-regulated genes ( mig-14 , pagC , and pagD ) also asymptotically reached the steady-state levels in the EG14943 strain , which is shown in fig .
The mig-14 genes appear to be regulated by both PhoP , by a mechanism .
To identify the PhoP-regulated gene ( s ) responsible for motility on 0.3 % agarose low Mg2 + media , we tested the behavior of strains mutated in each of 19 different PhoP-activated genes ( mgtA , mgtB , mgtC , mig-14 , pagC , pagK , pagM , pagN , pagO , pagP , pcgL , pgtE , phoN , pmrD , rstA , slyA , ugtL , virK , and yobG ) .