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. Author manuscript; available in PMC: 2014 Jul 23.
Published in final edited form as: Mol Microbiol. 2012 Oct 17;87(3):478–492. doi: 10.1111/mmi.12052

Fig. 2.

Fig. 2

In vivo effects of mutations in IscR binding sites A, B, and C within PiscR. β-galactosidase activity from wild-type (PK7571) or mutated (PK8521, PK8528, PK8582, PK8551, PK8801, PK8808, PK8820) PiscR-lacZ fusions (recombined at the chromosomal lac region) was measured in cells grown under A) aerobic or B) anaerobic conditions in MOPS minimal media with glucose (0.2%). The amount of IscR-dependent repression (Fold repression) was determined by dividing the β-galactosidase activity present in the strain lacking IscR (PK7572) by the β-galactosidase activity measured for each strain. The presence (+) or absence (−) of wild-type IscR binding sites A, B, and C in the PiscR-lacZ fusion is indicated below the figure. Error bars represent the propagation of standard errors for three biological replicates.