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. 2012 Apr 12;287(23):19284–19293. doi: 10.1074/jbc.M112.344903

FIGURE 4.

FIGURE 4.

SOD activity is required for resistance to streptonigrin. A, ML23/pBBE22, sodA/pBBE22, and complemented strains were inoculated into BSK-II medium containing nothing, dimethyl sulfoxide (control, DMSO), or streptonigrin (10 μg ml−1, SN), and growth was monitored over time. The data are from separate experiments with different batches of BSK-II medium (n = 5). An asterisk indicates a significant difference, corrected with Bonferroni correction, in the final cell density of the sample compared with streptonigrin compared with the parental strain with streptonigrin (p < 0.025). B, schematic and confirmation of the generation of ΔsodA in a B31-A3 background (strain BT002). sodA::aadA was transferred from ΔsodA in the ML23 strain as described under “Experimental Procedures” (left panel). PCR with primers 1 and 3 confirmed the insertion of the aadA marker within the coding region of sodA. Lane 1, B31-A3; lane 2, strain BT002 (ΔsodA). The ∼2.3-kb DNA fragment corresponds to sodA::aadA, whereas the 0.7-kb DNA fragment is present in the parental strain B31-A3 (right panel). C, growth of B31-A3 with 300 μm dip in the presence or absence of streptonigrin (10 μg ml−1). Growth was monitored over time by cell enumeration with dark field microscopy. An asterisk indicates significant difference in the final cell density of sample with dip and streptonigrin compared with the parental strain with dip and streptonigrin (p < 0.05).