Hypoviral‐regulated HSP90 co‐chaperone p23 (CpCop23) determines the colony morphology, virulence, and viral response of chestnut blight fungusCryphonectria parasitica

Abstract

AbstractWe previously identified a protein spot that showed down‐regulation in the presence of Cryphonectria hypovirus 1 (CHV1) and tannic acid supplementation as a Hsp90 co‐chaperone p23 gene (CpCop23). TheCpCop23‐null mutant strain showed retarded growth with less aerial mycelia and intense pigmentation. Conidia of theCpCop23‐null mutant were significantly decreased and their viability was dramatically diminished. TheCpCop23‐null mutant showed hypersensitivity to Hsp90 inhibitors. However, no differences in responsiveness were observed after exposure to other stressors such as temperature, reactive oxygen species, and high osmosis, the exception being cell wall‐disturbing agents. A severe reduction in virulence was observed in theCpCop23‐null mutant. Interestingly, viral transfer to theCpCop23‐null mutant from CHV1‐infected strain via anastomosis was more inefficient than a comparable transfer with the wild type as a result of decreased hyphal branching of theCpCop23‐null mutant around the peripheral region, which resulted in less fusion of the hyphae. The CHV1‐infectedCpCop23‐null mutant exhibited recovered mycelial growth with less pigmentation and sporulation. The CHV1‐transfectedCpCop23‐null mutant demonstrated almost no virulence, that is, even less than that of the CHV1‐infected wild type (UEP1), a further indication that reduced virulence of the mutant is not attributable exclusively to the retarded growth but rather is a function of theCpCop23gene. Thus, this study indicates thatCpCop23plays a role in ensuring appropriate mycelial growth and development, spore viability, responses to antifungal drugs, and fungal virulence. Moreover, theCpCop23gene acts as a host factor that affects CHV1‐infected fungal growth and maintains viral symptom development.