Abstract
THE soil-borne fungus Fusarium oxysporum causes wilt in many economically important host plants and, like many plant pathogenic fungi, it consists of several specialized forms, each including a number of pathogenic races. A striking feature of Fusarium wilts is their sudden occurrence in crops in which they were previously unknown1,2. Such new disease outbreaks clearly suggest that either saprophytic forms of the fungus have become parasitic or that existing parasitic races have extended their host-range. Among genetic mechanisms already proposed to explain such changes of pathogenicity in Fusarium and other imperfect fungi are mutation, heterokaryosis, which allows haploid nuclei to associate in various ways, and a parasexual mechanism3, which allows permanent genetic recombination without a sexual stage4. On the other hand, there is some evidence that pathogenicity can be influenced by the host. For example, Reddick and Mills5 increased the varietal host range of Phytophthora infestans by successively transferring haploid zoospore cultures on to a series of potato varieties of increasing resistance to this fungus. Bawden6, in discussing the role of plant hosts in microbial ecology, pointed out that this approach can be extended by first correlating the mechanism of resistance with the presence in the host of some toxin specific to the fungus pathogen or with the lack of some metabolite essential for its growth.
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References
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BUXTON, E. A Change of Pathogenic Race in Fusarium oxysporum f. pisi induced by Root Exudate from a Resistant Host. Nature 181, 1222–1224 (1958). https://doi.org/10.1038/1811222b0
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DOI: https://doi.org/10.1038/1811222b0
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