Fig. 5: A point mutation in a core catalytic residue of ACE1 abolishes not only the recognition by rice Pi33 but also the aggressiveness on wheat.

a Pathogenicity of MoO isolate PO12-7301-2 (PO), its transformants carrying intact ACE1^Br48 fused to a GFP gene (PO + ACE1^Br48:GFP), and those carrying ACE1^Br48 with the C183A mutation fused to a GFP gene (PO + ace1^BrC183A:GFP) on fourth leaves of rice cv. Aichi–Asahi (pi33) and cv. Bala (Pi33) and primary leaves of barley cv. Nigrate. Similar results were obtained in two independent experiments. b Pathogenicity of MoT isolate Br48, its ACE1-knockout mutant Br48ΔACE1 (#112), and transformants of Br48ΔACE1 (#112) carrying intact ACE1^Br48 fused to a GFP gene (Br48ΔACE1 + ACE1^Br48:GFP), and those carrying ACE1^Br48 with the C183A mutation fused to a GFP gene (Br48ΔACE1 + ace1^BrC183A:GFP) on primary leaves of wheat cv. N4. The boxplot shows the percentage of lesion area in three independent experiments. N = 26 (for Br48ΔACE1 + ACE1^Br48:GFP #G16 and Br48ΔACE1+ace1^BrC183A:GFP #M11) or 27 (for the other strains) biologically independent samples. Center lines show the medians; box limits indicate the 25th and 75th percentiles; whiskers extend to 1.5x the interquartile range from the 25th and 75th percentiles. Different letters indicate significant differences determined by Dunn’s test at the 5% level. Inoculated leaves were incubated at 26 °C (rice) or 22 °C (barley and wheat) for 5 days.