MoCrn1 contributes to pathogenicity by regulating cAMP levels.

(A) Pathogenicity assay was conducted by spraying conidial suspensions (5×104 conidia/ml) onto two-week old rice seedlings (CO-39). Mean number of lesions per 5 cm length of leaf were quantified. Expressing MoMagAG187S in ΔMocrn1 suppressed the defects in infection. (B) Penetration assays with rice sheath tissues. Micrographs show the percentages of 4 types of IH observed at 36 hpi. Bars = 10 μm. 1 or 2 mM 8-Br-cAMP addition could promote penetration for ΔMocrn1. (C) Pathogenicity assay was conducted with detached barley leaves. Addition of 1 mM and 2 mM 8-Br-cAMP enhanced ΔMocrn1 infection. (D) Bar chart shows the intracellular cAMP levels in mycelium of the strains. (E) Mutation of H29D and CC deletion for MoCrn1 caused defects in pathogenicity. Quantification for the lesions per 5 cm length of leaf is given. (F and G) Bar charts show the percentages of appressoria containing glycogen and lipids at different time points. The ΔMocrn1 mutant, ΔMocrn1/MoCRN1H29D and ΔMocrn1/MoCRN1ΔCC strains delayed the degradation of glycogen and lipids. Asterisks in (D) and (E) represent significant differences (P<0.01).