Extended Data Fig. 7: PrdR is over-expressed in VREfm with RpoB substitutions.
From: Rifaximin prophylaxis causes resistance to the last-resort antibiotic daptomycin

a. Intersection between RNAseq and proteomics analyses displayed as an UpSet plot (n = 5 independent biological replicates for RNAseq and n = 5 independent biological replicates for proteomics). The bar represents the count of each locus that was identified in each sample. RNA seq significance (FDR < 0.05, log2FC > 1 or log2FC < −1) and proteomics significance (adjusted p-value < 0.05, log2FC > 1 or log2FC < −1). b. Locus map of the prdR locus in the VREfm AUS0233 genome ([proteins] AGS74325, AGS74326, AGS74327 or EFAU233_00444, EFAU233_00445, EFAU233_00446). c. Proteomics comparing the abundance of the PrdRAB locus across five different clinical strain pairs (n = 5 independent biological replicates for each strain). Bars are the fold-change (log2) from five independent biological replicates showing proteins with statistically significant (<0.05) P-values. The y-axis is the log2 fold-change. Data was analysed using an unpaired t-test of daptomycin-susceptible clinical strain versus daptomycin-resistant clinical strain (with a RpoB mutation). d. Protein abundance changes of the clinical VREfm strain pairs (n = 5 independent biological replicates each isolate) containing mutations in RpoB from different genetic backgrounds, demonstrating the conserved upregulation of the PrdRAB operon. The x-axis is the log2 fold-change and the y-axis is the -log10 P value.