Fig. 5: PopP2 K383, L369/V370, and L371/D372 residues are required for activation of RRS1-R-dependent immunity.
From: Secondary-structure switch regulates the substrate binding of a YopJ family acetyltransferase
a Pseudomonas fluorescens (Pf0-1)-delivered PopP2 mutants K383A, L369P/V370P, and L371P/D372P trigger an attenuated RRS1-R-dependent cell death response in Ws-2 accession, compared to WT PopP2. Four-week-old Arabidopsis leaves were infiltrated with Pf0-1 strains delivering the indicated PopP2 proteins (WT PopP2, PopP2C321A, PopP2L369P/V370P, PopP2L371P/D372P, PopP2R380A, and PopP2K383A). The photographs were taken at 72 h post infection (hpi), although the cell death response was already visible at 24 hpi. The numbers in brackets indicate the proportion of leaves developing a cell death response (HR hypersensitive response). The asterisk indicates a weaker HR observed compared to WT PopP2. This experiment was conducted three times with similar results. b Integrity of PopP2 L369/V370, L371/D372, and K383 residues is required for PopP2-triggered ion leakage in Ws-2. Data are mean ± SE (n = 4) of one representative experiment. Graphs indicate the ratio between released ions at each time point over total ion level measured at the end of the experiment upon sample boiling (relative conductivity). This experiment was conducted three times with similar results.
