Regulatory pathways governing modulation of fungal gene expression by a virulence-attenuating mycovirus.

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A viral double-stranded RNA associated with virulence attenuation (hypovirulence) in the chestnut blight fungus (Cryphonectria parasitica) has been shown by DNA-mediated transformation to be responsible for transmissible hypovirulence. In addition to reduced virulence, the fungal strain harboring this virus exhibits a diverse array of characteristics, termed hypovirulence-associated traits, which distinguish it from an isogenic virus-free strain. We have investigated one of these traits, suppressed lac-1 (laccase) transcript accumulation. Two different and opposing regulatory pathways appear to govern lac-1 transcript levels in the virus-free strain: a stimulatory pathway was found to be dependent on the inositol trisphosphate (IP3) and calcium second messenger systems. A second pathway limiting transcript accumulation was shown to require ongoing protein synthesis. Additionally, changes in the level of lac-1 transcript accumulation were found to be related to modulation of promoter activity and this activity was shown to be suppressed in the virus-containing strain. We conclude that this hypovirulence-associated virus interferes with transduction of an IP3-calcium-dependent signal that is required for stimulation of lac-1 transcription. The perturbation of such signal transduction pathways by hypovirulence-associated viruses may account for the manifold symptoms associated with transmissible hypovirulence.

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