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Downy mildew of sunflower (Plasmopara halstedii) can be effectively controlled by either genetic resistance or chemical pesticides but the development of new pathogen genotypes may lead to a re-emergence of the disease. The aim of the present work was to determine whether chemical inducers of disease resistance such as dichloroisonicotinic acid (INA) and β-aminobutyric acid (BABA) induce resistance to downy mildew in susceptible sunflowers, and affect resistant responses in mildew-inoculated resistant sunflower lines. Treatments of 3-day-old seedlings with one of these chemicals significantly reduced downy mildew disease symptoms (sporulation, stunting) in susceptible plants, and inhibited systemic mycelial growth of the pathogen. Furthermore, host cellular responses, like necrosis and secondary cell division became evident at infection sites. These effects are similar to those found in previous studies with benzothiadiazole, and closely resemble defense responses in sunflower plants carrying P. halstedii resistance genes. Under in vitro conditions, these activators slightly inhibited the germination of zoosporangia.

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