Fig. 5

SAGA complex is essential for DON biosynthesis and virulence in Fg. a Pathogenicity of six gene deletion mutants of the SAGA complex on wheat heads. b Toxisome formation in the hyphae of ΔFgPCN, ΔFgADA3, and ΔFgGCN5 and wild-type strains under PCN treatment at 15 and 25 µg ml⁻¹. Tri1-GFP was used as the toxisomal marker for observation. The chemical fungicide carbendazim (abbreviated as Car) at the EC90 concentration, 1.4 µg ml⁻¹, was used as a control treatment; bar = 10 µm. c Expression of Tri1-GFP in tested mutants and the wild type treated with PCN or Carbendazim was verified by immunoblot assays using the anti-GFP antibody. In addition, the protein samples were also detected with the monoclonal anti-GAPDH antibody as a reference. d Deoxynivalenol (DON) production in the mutants and the wild type treated with PCN or carbendazim. DON in cell-free supernatants after 4 days of incubation in TBI medium were harvested, extracted, and quantified by LC-MS. Data presented are the mean ± s.d. (n = 3). e Toxisome formation in the hyphae of ΔFgPCN, ΔFgADA3, and ΔFgGCN5 mutants and wild-type labeled with Tri1-GFP inoculated on wheat leaf; bar = 40 µm. f Penetration structures of wild-type, ΔFgPCN, ΔFgADA3, and ΔFgGCN5 strains on dissected wheat glumes at 72 h post inoculation. Red arrows indicate the typical infection structures of the fungus