Role of Mitochondrial DNA in the Senescence and Hypovirulence of Fungi and Potential for Plant Disease Control

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Abstract
The unique coenocytic anatomy of the mycelia of the filamentous fungi and the formation of anastomoses between hyphae from different mycelia enable the intracellular accumulation and infectious transmission of plasmids and mutant mitochondrial DNAs (mtDNAs) that cause senescence. For reasons that are not fully apparent, mitochondria that are rendered dysfunctional by so-called “suppressive” mtDNA mutations proliferate rapidly in growing cells and gradually displace organelles that contain wild-type mtDNA molecules and are functional. The consequence of this process is senescence and death if the suppressive mtDNA contains a lethal mutation. Suppressive mtDNA mutations and mitochondrial plasmids can elicit cytoplasmically transmissible “mitochondrial hypovirulence” syndromes in at least some of the phytopathogenic fungi. In the chestnut-blight fungus Cryphonectria parasitica, the pattern of asexual transmission of mutant mtDNAs and mitochondrial plasmids resembles the pattern of “infectious” transmission displayed by the attenuating virus that is most commonly used for the biological control of this fungus. At least some of the attenuating mitochondrial hypovirulence factors are inherited maternally in crosses, whereas the viruses are not transmitted sexually. The natural control of blight in an isolated stand of chestnut trees has resulted from the invasion of the local population of C. parasitica by a senescence-inducing mutant mtDNA. Moreover, a mitochondrial plasmid, pCRY1, attenuates at least some virulent strains of C. parasitica, suggesting that such factors could be applied to control plant diseases caused by fungi.