| Research Abstract |
The soil-borne fungus Fusarium oxysporum causes vascular wilts of a wide variety of plant species by directly penetrating roots and colonizing the vascular tissue. Individual pathogenic strains within the species have a limited host range, and strains similar or identical host ranges are assigned to intraspecific groups, called formae speciales (f.sp.). We previously isolated 43 pathogenicity mutants of the melon wilt pathogen F.oxysporum f. sp. Melonis by restriction enzyme-mediated DNA integration mutagenesis. In this research, we analyzed the structures and functions of tagged sites in the mutants to isolate genes required for pathogenicity and symptom development by this pathogen.
We identified the mutated genes, named AGR1, FOW1, FOW2, FOW3, and FOW4, from five mutants. Essential roles of these genes in full pathogenicity of this pathogen were confirmed by genetic complementation and transformation-mediated targeting experiments. These genes possibly encode argininosuccinate lyase, mitochondrial carrier protein, Zn(II)2Cys6 transcription factor, Cys2His2 transcription factor, and phosphoenoylpyruvate carboxykinase, respectively, and are novel pathogenicity genes of plant pathogenic fungi.
FOW2 and FOW3 encode different transcription regulators, suggesting that they regulate expression of the genes directly involved in pathogenicity. In this research, we isolated a Fow2-regulated gene, named F2R1, by subtraction of cDNAs of the wild-type strain with those of the fow2 mutant. F2R1 encodes a protein similar to cytokine-regulated glycoprotein of the animal pathogen Cryptococcus neoformans. The f2r1 mutant showed slightly reduced virulence to melon plants, although the fow2 mutant completely lost pathogenicity. These results suggest that Fow2 regulates expression of multiple pathogenicity genes, including F2R1.
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