Abstract

Host infection by Magnaporthe oryzae requires the formation of a specialized infection structure, the appressorium. Using yeast 2-hybrid, ACI1 was found to interact with MAC1, a key gene in the cAMP signaling pathway regulating appressorium formation. Targeted ACI1 gene replacement mutants exhibited significantly delayed and slightly lower levels of appressorium formation, but were indistinguishable from the wild type strain in terms of pathogenicity. No differences were observed in colony morphology and wettability, growth rate, conidiation and salt tolerance. These results suggest that the ACI1 is required for normal appressorium formation, but not for pathogenicity and vegetative growth. Characterization elsewhere of an ACI1 homologue IMR gave similar results. Functional redundancy resulting from the presence of related homologues in the M. oryzae genome is one explanation that may account for these findings.

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