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Botrytis cinerea, a cosmopolitan nectrotrophic fungus, is the cause of gray mold in a wide range of crops including grapevine, where it affects both fruit quality and yield. The pathogen is difficult to manage due to the quiescent state of infection ensuing after the primary infection. Primary infection mostly occurs at bloom by airborne conidia; and the fungus remains quiescent until maturity and egresses at ripe to causes bunch rot. To understand the molecular crosstalk between the grapevine and B. cinerea during initial infection and entrance into quiescence, inflorescences of Vitis vinifera (cv. Pinot Noir) were inoculated with B. cinerea at anthesis. Infections were halted at 12, 24, 48, 72 and 96 hours post inoculation (hpi) and samples were subjected to confocal microscopy, quantitative polymerase chain reaction and RNA-sequence analyses. It was observed that most of the conidia germinated and form apressoria-like structures within 24 hpi, which resulted in penetration of the flower epidermis. During penetration, B. cinerea increased the expression of its genes encoding for virulence factors that instigated defense responses from the flowers side. The defense responses involved genes associated with the accumulation of pathogenesis-related proteins, stilbenoids, reactive oxygen species and cell wall reinforcement. At 96 hpi the transcriptional reaction appeared largely diminished both in the host and in the pathogen, implying B. cinerea became quiescent, forced by the defense responses of the host, until conditions favor egression. |
