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  • Author or Editor: Wojciech J. Janisiewicz x
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William S. Conway, Wojciech J. Janisiewicz, Joshua D. Klein and Carl E. Sams

The viability of Penicillium expansum Link conidia in sporulating culture declined rapidly when exposed to 38 °C, and when conidia were exposed to 38 °C prior to inoculation of apple fruits (Malus ×domestica Borkh.), the resulting lesions were smaller than those on fruit inoculated with nonheated conidia. `Gala' apples were heated after harvest (38 °C for 4 days), pressure infiltrated with a 2% solution of CaCl2, or treated with the antagonist Pseudomonas syringae van Hall, alone or in combinations to reduce postharvest decay caused by Penicillium expansum. After up to 6 months in storage at 1 °C, no decay lesions developed on fruit that were heated after inoculation with P. expansum, or any combination of P. expansum, antagonist, or Ca. Parallel lots of heat-treated and nonheated fruit that were either infiltrated or not infiltrated with Ca were stored up to 6 months. They were then inoculated with P. expansum alone, or with the antagonist followed by P. expansum. Prior heat treatment did not influence lesion size. Calcium alone, the antagonist alone, and heat plus Ca all reduced the incidence of decay by ≈25%, whereas heat plus the antagonist reduced it by 70%. Calcium plus the antagonist or Ca plus the antagonist and heat reduced decay incidence by 89% and 91%, respectively. The integrated strategy of heat-treating fruit, followed by Ca infiltration and then treatment with an antagonist, may be a useful alternative to controlling postharvest decay with fungicides.

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Wojciech J. Janisiewicz, Robert A. Saftner, William S. Conway and Philip L. Forsline

Blue mold of apples, incited by Penicillium expansum, causes extensive losses on stored apples worldwide. Despite the severity of this problem, apple breeders do not evaluate their crosses for resistance to this disease, because there has been little resistance to blue mold in the gene pool of the germplasm used. A new apple germplasm collection from the center of origin in Kazakhstan, maintained in Geneva, NY, and representing a much broader gene pool, was evaluated for resistance to blue mold. Apples were harvested from the Elite collection trees that were clonally propagated from budwood collected in Kazakhstan and from seedling trees originating from seeds of the same trees as the Elite budwood or from other wild seedling trees in Kazakhstan. Fruit from 83 such accessions were harvested at the preclimacteric to climacteric stage, wound-inoculated with P. expansum at 103, 104, and 105 mL−1 conidial suspension, incubated for 5 d at 24 °C, and evaluated for decay incidence and severity. Two accessions were classified as immune (no decay at 103 and 104 mL−1), four as resistant (no decay at 103 mL−1), 53 as moderately resistant (lesions less than 10 mm at 103 mL−1), and 24 as susceptible. There were positive correlations (r = 0.92, 0.86, and 0.91) between decay severity and all three inoculum levels. Our results indicate a greater genetic diversity among the Kazak apple collection than among cultivated apples as evidenced by their broad range of fruit maturity, quality, and disease resistance patterns. The immune and resistant accessions may serve as a source of resistance in breeding programs and can be useful in explaining the mechanism of resistance to blue mold in apples.