Abstract

AbstractThe ascomycete fungus Botryosphaeria dothidea is the causal agent of postharvest rot in kiwifruit. Production and spreading of conidia, differentiation of infection hyphae and invasion of intact fruit surfaces are required to cause fruit rot disease. In several pathogenic fungi, the homologue of the Saccharomyces cerevisiae mitogen activated protein kinase (MAPK) gene Fus3 has been identified as a pathogenicity factor. To investigate the role of the Fus3 homologue in B. dothidea, the gene was deleted and the resulting ∆fus3 mutants were characterized. On artificial media, strong growth defects of ∆fus3 strains were observed, mycelia were non‐pigmented, and mutants were unable to conidiate. Scanning electron microscopy showed that the wild‐type strain differentiated thick hyphae on the surface of kiwifruits, and nose‐down growth of hyphae indicated tight attachment to the fruit. In contrast, hyphae of ∆fus3 strains mutants were thinner and did not firmly attach to the fruit surface. Importantly, pathogenicity test revealed that ∆fus3 strains were unable to cause disease symptoms on intact kiwifruits. These results shown here identify Fus3 of B. dothidea as a novel pathogenicity factor of the ripe rot pathogen on kiwifruit.

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