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The remaining PMs mutants ( surA and tolB ) , as well as the two PmrA-regulated gene ( yibD and dgoA ) mutants , retained aminoarabinose on lipid-A .
yibD , dgoA , and gnd ( likely affecting pmrE ) played no role in PmrA-regulated resistance to high iron concentrations , while surA and tolB mutations grew poorly on high iron media .
While it is possible that these PmrA-regulated genes ( as well as the genes involved in PM resistance ) could affect the other known PmrA-induced LPS modification , pEtN , we feel that this is unlikely based on what is known about the identified genes ( surA , tolB , and pmrE ) and because yibD and dgoA do not affect virulence or PM resistance , which are predicted phenotypes of the loss of pEtN modification from the core ( 59 ) .