As a high value ornamental plant, Paphiopedilum micranthum is planted in many provinces in China. In December 2018, a leaf spot disease on P. micranthum was observed in the gardens of Leye County (...

Curvularia lunata (Wakkre) Boedijn is an important pathogenic fungus that causes maize leaf spot, a prevalent disease that caused significant yield losses in maize-growing areas in China in the 1990s. Clpks18, a polyketide synthase (CLPKS18) gene, has been identified as a crucial virulence-related gene in C. lunata. However, the impact of Clpks18 and its biosynthesized virulence factor (R)-(-)-mellein on the expression of maize genes related to the defense signal pathway has never been determined. In this study, it was found that Clpks18 and (R)-(-)-mellein significantly interfere with the signaling pathways of JA and IAA in maize leaves but in different ways and in a time-dependent manner. While CLPKS18 inhibited the maize’s JA and IAA signaling pathways through its related secondary metabolite, (R)-(-)-mellein inhibited the JA signaling pathway but stimulated IAA accumulation in maize leaves. In summary, understanding this novel virulence effector’s mechanism of interference with maize resistance enriches the pathology of Curvularia leaf spot in maize on the one hand and provides a foundation for screening the resistance germplasm and chemical fungicides against the disease on the other.

Maize leaf spot, which is caused by Curvularia lunata (Wakkre) Boedijn, was epidemic in the maize-growing regions of northeastern and northern China in the mid-1990s, where it led to large yield losses. Since then, the epidemic has evolved into a kind of common disease. In recent years, however, a tendency of becoming an epidemic disease again has been observed in some areas in China due to significant changes in climate, farming, systems and crop varieties. The significance of methyl-(5hydroxymethyl) furan-2-carboxylate (M5HF2C) as a nonspecific host toxin in causing maize leaf spot disease has been demonstrated in previous research. However, the key enzymes involved in M5HF2C toxin synthesis remain unclear. In our study, we demonstrate that the synthesis of M5HF2C toxin starts from a precursor substrate in the pathogen, furfural, which is then catalytically dehydrogenated into furoic acid via an alcohol dehydrogenase (CLADH6). The furoic acid was further confirmed as one of the raw materials for the biosynthesis of M5HF2C toxin based on deletion mutants of the alcohol dehydrogenase gene (Cladh6) in C. lunata, which had reduced M5HF2C toxin-producing ability; however, this ability could be restored in all deletion mutants through complementation with furoic acid, thereby confirming that furoic acid is an intermediate in the biosynthesis of M5HF2C toxin. In summary, the biosynthesis process of M5HF2C toxin in C. lunata involves three transformation steps: (1) from xylose to furfural; (2) then from furfural to furoic acid; and (3) eventually from furoic acid to M5HF2C toxin. Our research findings provide new clues in elucidating the major steps in the process of M5HF2C toxin biosynthesis in C. lunata.