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dc.contributor.authorThomas, Sara
dc.description.abstractThe specialized fungal pathogen Monilinia vaccinii-corymbosi infects blueberry flowers via the gynoecial pathway causing mummy berry disease. Managing flower infections is hampered by the short window for well-timed management and the rapid appearance of new infection courts (open flowers) during bloom. Induced resistance (IR) may offer a solution to this challenge, but limited information is available about IR responses in flower pathosystems. Using tomato as a model, treatment with methyl jasmonate (MeJA) and benzothiadiazole (BTH) resulted in overexpression in flower pistils of the IR marker genes Pin2 and PR-4 by 5.17 and 5.62-fold, respectively. In blueberry, PR-3 and PR-4 orthologs were first identified and characterized as IR genes using in silico and wet-lab techniques. In subsequent flower induction studies, 2,6-dichloroisonicotinic acid (INA) and BTH induced overexpression of PR-4 by 3.18 and 1.75-fold, respectively. When treated tomato and blueberry flowers were challenged with the respective pathogens, Botrytis cinerea and M. vaccinii-corymbosi, no disease suppression was observed. Thus, although IR marker genes were inducible in floral tissue, the magnitude of this effect was insufficient to control infection. Hence, other strategies, such as optimizing efficacy of conventional fungicides, are needed. Current fungicidal management of M. vaccinii-corymbosi relies on multiple sprays during bloom to ensure that the stigma is exposed to active ingredient. However, flowers that open between applications remain unprotected, unless there is systemic movement and/or eradicant activity of active ingredient in the pistil. The activity in floral tissue of two systemic fungicides, fenbuconazole and triforine, was assessed in greenhouse experiments where a single fungicide application was made to plants having multiple pre- and post-anthesis flower stages. Flowers were inoculated 1 day after anthesis, and subsequent fruit mummification recorded. Both fungicides provided excellent protection to flowers at anthesis during fungicide application. Fenbuconazole also protected flowers up to 2 days before and 2.5 days after anthesis, giving a 4.5-day protection window. In contrast, triforine was effective for 11.5 days, extending from 5 days before to 6.5 days after anthesis. Prevention of ovary colonization by eradicant activity appeared to be the predominant mode for superior activity of triforine against M. vaccinii-corymbosi in flowers.
dc.subjectVaccinium virgatum
dc.subjectMummy berry
dc.subjectMonilinia vaccinii-corymbosi
dc.subjectFlower infection
dc.subjectInduced resistance
dc.subjectPathogenesis-related genes
dc.subjectDMI fungicide
dc.titleManagement of blueberry flower infection by Monilinia vaccinii-corymbosi
dc.title.alternativepotential for induced resistance and pre- and post-anthesis fungicide activity
dc.description.departmentPlant Pathology
dc.description.majorPlant Pathology
dc.description.advisorHarald Scherm
dc.description.committeeHarald Scherm
dc.description.committeeHazel Wetzstein
dc.description.committeeRonald R. Walcott
dc.description.committeeJames Leebens-Mack

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