Abstract

Setosphaeria turcica f. sp. zeae and S. turcica f. sp. sorghi cause northern leaf blight of corn and sorghum, respectively. As two formae speciales of S. turcica , they have obvious physiological differentiation and show complete host specificity. Host specificity is often closely related to pathogen virulence factors, including secreted protein effectors and secondary metabolites. S. turcica f. sp. zeae had fewer predicted secreted proteins, pathogen-host interaction (PHI) genes and carbohydrate-active enzymes (CAZymes) than S. turcica f. sp. sorghi . Fifteen and 20 polyketide synthase (PKS) genes were identified in S. turcica f. sp. zeae and S. turcica f. sp. sorghi , respectively, which maintained high homology. There were 8 functionally annotated effector protein-encoding genes specifically in S. turcica f. sp. zeae , among which the encoding gene StCEL2 of endo-1,4-β- d -glucanase, an important component of cellulase, was significantly up-regulated during the interaction process. Finally, gluconolactone inhibited cellulase activity and decreased infection rates and pathogenicity, which indicates that cellulase is essential for maintaining virulence. These findings demonstrate that cellulase plays an important role in the pathogenicity of S. turcica f. sp. zeae .

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