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. 2022 Aug 1;18(8):e1010331. doi: 10.1371/journal.pgen.1010331

Fig 7. STPK phosphorylation of PrrA is critical for Mtb entry into an adaptive state of growth arrest upon extended NO exposure.

Fig 7

(A) Blocking STPK phosphorylation of PrrA affects the ability of Mtb to enter a state of growth arrest upon extended NO exposure. PrrA-DUC/ΔprrA (“WT”) and PrrA-T6A-DUC/ΔprrA (“T6A”) were treated with 4 doses of 100 μM DETA NONOate over 30 hours (red shaded region indicates period of treatment) and growth tracked over time. Data are shown as means ± SD from 3 experiments. p-values were obtained with an unpaired t-test, comparing PrrA-T6A-DUC/ΔprrA to PrrA-DUC/ΔprrA within each condition. * symbols indicate p-values for the untreated conditions. # symbols indicate p-values for the NO conditions. * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001. (B) The PrrA-T6A variant is more sensitive to isoniazid. Log-phase PrrA-DUC/ΔprrA ("WT") and PrrA-T6A-DUC/ΔprrA (“T6A”) Mtb were treated with isoniazid (INH) for 24 hours. Percent survival compares the number of CFUs from each INH treatment to the untreated control condition for each strain. Data are shown as means ± SD from three experiments. p-values were obtained with an unpaired t-test.