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. 2019 Aug 20;47(18):9658–9665. doi: 10.1093/nar/gkz721

Figure 2.

Figure 2.

Aca2 represses the acrIF8–aca2 operon. (A) Schematic of the plasmid setup for the assay to measure autoregulation of the acrIF8–aca2 promoter by Aca2 in a Pca ZF40– host (Pca RC5297). (B) Activity of acrIF8–aca2 promoter variants in Pca ZF40– in the presence and absence of Aca2, determined as the median eYFP fluorescence. The IR sites were mutated as indicated; sc: scrambled or Δ: deleted. (C) Schematic of the acrIF8–aca2 promoter assay in the ZF40+ strain (Pca lysogen ZM1). (D) Activity of acrIF8–aca2 promoter variants in the Pca ZF40+ strain, determined as the median eYFP fluorescence. The Pca ZF40– control strain lacks aca2 and in the Pca ZF40+ strain aca2 is expressed natively from the ZF40 prophage. (E) Activity of acrIF8–aca2 promoter variants in the Pca ZF40– strain in the presence of different concentrations of arabinose to induce aca2 expression. In (B) and (D), data are presented as the mean ± standard deviation of four biological replicates and statistical significance was tested by two-tailed unpaired t-tests (*P < 0.05, ***P < 0.001). In (E), data are presented as the mean ± standard deviation of six biological replicates and statistical significance compared to the wtIR1-wtIR2 promoter was tested by two-way ANOVA with Dunnett's Multiple Comparisons Test (***P < 0.001, ns: P > 0.05).