23 research outputs found

    Elicitation of resistance and defense related proteins by î²-amino butyric acid in sunflower against downy mildew pathogen plasmopara halstedii

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    Induction of resistance to downy mildew caused by Plasmopara halstedii in sunflower was studied after treatment with b-amino butyric acid (BABA). Treatment of sunflower seeds with 50 mM BABA resulted in decreased disease severity and offered 47 and 50% protection under greenhouse and field conditions, respectively. The induction of resistance to P. halstedii by BABA was accompanied by the accumulation of various host defense related enzymes in susceptible sunflower seedlings. Enhanced activation of catalase, phenylalanine ammonia-lyase (PAL), chitinase (Pr3), peroxidase (POX), and polyphenol oxidase (PPO) was evident at 6 h, 9 h, 12 h, 12 h and 12 h post-inoculation, respectively in sunflower seedlings raised from seeds treated with BABA. Northern hybridisation analysis revealed increased levels of transcripts for five known defense-response genes, viz chalcone synthase, Pr-1a, peroxidase, b-1,3-glucanase and chitinase in these seedlings. This enhanced and early activation of defense related responses in the susceptible cultivar after treatment with BABA was comparable to that in the resistant cultivar. The results indicate that BABA-induced resistance against P. halstedii in sunflower is mediated through enhanced expression of genes for defense related proteins

    Chitosan induced resistance to downy mildew in sunflower caused by Plasmopara halstedii

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    Induction of resistance to downy mildew caused by Plasmopara halstedii in sunflower was studied after treatment with chitosan. Treatment of sunflower seeds with 5 chitosan resulted in decreased disease severity and offered 46 and 52 protection under greenhouse and field conditions respectively. The induction of resistance to P. halstedii by chitosan was accompanied by the accumulation of various host defense-related enzymes in susceptible sunflower seedlings. Enhanced activation of catalase (CAT) and phenylalanine ammonia lyase (PAL) was observed at 6h and 9h post-inoculation respectively, while peroxidase (POX), polyphenol oxidase (PPO) and chitinase (CHI) levels were high at 12h post-inoculation in sunflower seedlings raised from seeds treated with chitosan. Northern hybridization analysis revealed increased levels of transcripts for five known defense response genes viz., Pr-1a, β-1,3-glucanase, chitinase, peroxidase and chalcone synthase in these seedlings. This enhanced and early activation of defense-related responses in the susceptible cultivar Morden treated with chitosan was comparable to that in the resistant cultivar. The results indicate that chitosan induced resistance against P. halstedii in sunflower is mediated through the enhanced expression of genes for defense-related proteins

    Induction of resistance against downy mildew on sunflower by rhizobacteria

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    Induction of resistance to downy mildew caused by Plasmopara halstedii in sunflower was studied after treatment with PGPR (plant growth promoting rhizobacteria) strain INR7 (Bacillus spp). Treatment of sunflower seeds with 1×10<SUP>8</SUP>cfu/ml of PGPR strain INR7 resulted in decreased disease severity and offered 51 and 54% protection under green house and field conditions, respectively. The induction of resistance to P. halstedii by PGPR strain INR7 was accompanied by the accumulation of various host defense-related enzymes in susceptible sunflower seedlings. Enhanced activation of catalase (CAT), phenylalanine ammonia-lyase (PAL), peroxidase (POX), polyphenol oxidase (PPO) and chitinase (CHI) was evident at 6, 9, 12, 12 and 12h post inoculation, respectively, in sunflower seedlings raised from seeds treated with PGPR strain INR7. This enhanced and early activation of defense-related responses in the susceptible cultivar after treatment with PGPR strain INR7 was comparable to that in the resistant cultivar. The results indicate that PGPR strain INR7 induced resistance against P. halstedii in sunflower is mediated through enhanced expression of defense mechanism
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