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. 2006 Sep;188(18):6483–6489. doi: 10.1128/JB.00636-06

FIG. 2.

FIG. 2.

AmrZ binds to the fleQ promoter. (A) Mutation of amrZ in AlgT+ P. aeruginosa abolishes fleQ binding activity. Lane 1, free fleQ promoter DNA; lane 2, AlgT+ extract (3 μg); lane 3, AlgT− extract (3 μg); lane 4, AlgT+ AlgB− extract (3 μg); lane 5, AlgT+ AlgR− extract (3 μg); lane 6, AlgT+ AmrZ− extract (3 μg). (B) Complementation of the amrZ mutant restores binding to fleQ promoter DNA. Lane 1, free fleQ promoter DNA; lane 2, AlgT+ extract (3 μg); lane 3, AlgT+ AmrZ− extract (3 μg); lane 4, extract derived from an AlgT+ AmrZ− strain complemented with amrZ (3 μg). (C) AmrZ binds to the fleQ promoter. Lane 1, free fleQ promoter DNA; lane 2, AlgT+ extract (3 μg); lane 3, AlgT+ AmrZ− extract (3 μg); lanes 4 to 9, increasing amounts of recombinant AmrZ (1, 5, 10, 25, 50, and 100 ng, respectively). (D) Mutation of critical residues abolishes the ability of AmrZ to bind to fleQ. Lane 1, free fleQ promoter DNA; lanes 2 to 4, increasing amounts of recombinant AmrZ (20, 40, and 60 ng, respectively); lanes 5 to 7, increasing amounts of recombinant AmrZ K18A (20, 40, and 60 ng, respectively); lanes 8 to 10, increasing amounts of recombinant AmrZ R22A (20, 40, and 60 ng, respectively).