Biochemical and Molecular Changes in Downy Mildew‐infected Sunflower Triggered by Resistance Inducers

Abstract

In the present study, the mechanism of resistance to Plasmopara halstedii, the downy mildew pathogen of sunflower, triggered by three resistance-inducing chemicals, benzo (1,2,3) thiadiazole-7-carbothioic acid S-methyl ester (BTH), DL-b-amino butyric acid (BABA) and 2,6-dichloroisonicotinic acid (INA), was investigated in susceptible, completely resistant and partially resistant sunflower genotypes. By applying P. halstediispecific primers, no detectable pathogen marker transcript accumulation was found in the infected but completely resistant sunflower hypocotyls; however, pretreatments with either of the three resistance inducers decreased the transcript accumulation in both the infected susceptible and the partially resistant lines. Benzothiadiazole pretreatment before inoculation considerably enhanced enzyme activities in the infected susceptible and the completely resistant genotypes but not in partially resistant plants. Pretreatment with resistance inducers before inoculation increased glutathione S-transferase, defensin and catalase transcript levels in the susceptible but decreased in the partially resistant plants. Our results indicate that the resistance-inducing chemicals can improve resistance in all of the sunflower genotypes to downy mildew and increase enzyme activities of peroxidase and polyphenol oxidase, as well as accumulation of mRNAs of glutathione S-transferase, defensin and catalase. However, it is important to emphasize that activation of these defence-related proteins did not correlate with the degree of resistance, but rather with the amount of necrotic tissues.

The chemical inducer, BTH (benzothiadiazole) and root colonization by mycorrhizal fungi (Glomus spp.) trigger resistance against white rot (Sclerotinia sclerotiorum) in sunflower

“…BTH has been shown to activate resistance in many crops against a broad spectrum of diseases such as powdery mildew in barley and wheat [11], pea rust [4] and Sclerotinia diseases in melon [5] and soybean [8]. Similar activity was found to occur in sunflower against downy mildew [3,14,24] and rust disease [20].…”

Pathogenic, morphological and genetic diversity in Plasmopara halstedii, the causal agent of sunflower downy mildew

“…These results are in accordance with our previous analysis on the comportment of FU in the growth chamber (SAKR, 2011a;SAKR et al, 2011). Thus our observation suggests that in inbred line FU, the development of the pathogen was slowed, and may be due to resistance mechanisms expressed by accumulation of QTL in sunflower cultivars or presence of resistance-inducing chemicals which improve resistance in sunflower genotypes to downy mildew and increase enzyme activities (KÖRÖSI et al, 2011). Differences in aggressiveness of P. halstedii isolates are indicated when isolates vary in the degree of damage that they can cause in sunflower plants (SAKR, 2011a, b andc, 2012;SAKR et al, 2011).…”

Advances in sunflower downy mildew research

“…In Hungary, investigations have been made on the expression of genes allegedly associated with resistance response by measuring the accumulation of the transcripts of glutathion-S-transferase (GST), defensin (PDF), and catalase (CAT) following treatments with benzothiadiazole (BTH), dichloroisonicotinic acid (INA), or beta-aminobutyric acid (BABA) and/or P. halstedii inoculation. Preliminary results revealed significant increases in the activity of these genes in the susceptible but not in the resistant sunflowers, whereas the results with the partially resistant (HLI-type) sunflower were contradictory (Körösi and Virányi 2008). Apart from the plant activators, mentioned above, Nandeeshkumar et al (2008a) reported about an enhanced and early activation of defence-related responses to downy mildew in a susceptible sunflower cultivar treated with chitosan.…”