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. 2020 May 4;11:2200. doi: 10.1038/s41467-020-15966-7

Fig. 3. A transitory boost of stringent response contributes to initiate the switch to intracellular persistence.

Fig. 3

a Quantitative real-time PCR of transcripts of stringent response regulators in intracellular persisters exposed to 50× MIC oxacillin for the indicated times. Data, expressed in fold change vs control samples (extracellular bacteria mixed with J774 cells lysate), are means ± SEM of three independent experiments. b Cfus recovered from macrophages infected by HG001 (WT) and its isogenic mutants and exposed to 50× MIC oxacillin, clarithromycin or moxifloxacin for 24 h. Data (expressed as reduction from the original inoculum) are means ± SEM of four independent experiments. The dotted line indicates the limit of detection. Statistical significance was determined by one-way ANOVA with Dunnett’s post-test. Oxacillin [OXA], clarithromycin [CLR], moxifloxacin [MXF]. c MA-plot of genes related to translation78. The graph displays the log2 Fold Change expression as a function of log2 Base Mean (mean expression signal across all samples). Typical members of the function are pointed and aminoacyl-tRNA synthetases are shown in black. The dotted line indicates the basal expression level in control samples. Statistical significance is based on adjusted P-value. d Rate of GFP synthesis in intracellular S. aureus. Macrophages were infected by non-induced bacteria for 24 h, with (persisters) or without (control) 50× MIC oxacillin, and then induced for GFP expression for the indicated periods. Data are means ± SEM of GFP signal from flow cytometric profiles from three independent experiments. a, b, d, Source data are provided as a Source Data file.