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. Author manuscript; available in PMC: 2020 Sep 19.
Published in final edited form as: Cell. 2019 Sep 12;179(1):205–218.e21. doi: 10.1016/j.cell.2019.08.020

Figure 5. HopBF1 targets plant HSP90 during P. syringae infection (Related to Figure S5).

Figure 5.

(A) N. benthamiana leaves were infiltrated with P. syringae DC3000D28E expressing HopBF1 and appropriate A. tumefaciens strain to transiently express HSP90, HSP90 S100F or YFP as a control. Overexpression of HSP90 accelerated tissue necrotization triggered by bacteria expressing HopBF1 but not the S100F mutant or YFP. Photographs show representative leaves made 3 or 6 dpi as indicated. The experiment was performed 5 times with similar results.

(B) N. benthamiana leaves were co-infiltrated with appropriate Agrobacterium strains to express the autoactive variant of RPM1 (D505V) with or without HopBF1 or the D154A and D169A inactive mutants. Co-expression of WT HopBF1 but not the mutants strongly inhibited tissue necrotization. Photographs of the representative leaves were taken 5 days post infiltration.

(C) Model depicting the mechanism of HopBF1-dependent suppression of the HR in plants during P. syringae infection. T3SS modified from (Deng et al., 2017). We propose that HopBF1 has evolved to phosphorylate and inactive HSP90 to 1) prevent activation of NB-LRR proteins that trigger the HR in plants and 2) cause host cell death.