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The evaluation of the potential for chlorine dioxide to prime plant defenses for a systemic acquired resistance in light red kidney bean plants inoculated with common bean bacterial wilt

Date

2015

Authors

Sandoval, Vanessa Marie, author
Newman, Steven, advisor
Ramsey, Craig, advisor
Pilon, Marinus, committee member
Qian, Yaling, committee member

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Abstract

The induction of plant defenses is a great preventative tool for greenhouse and nursery managers to protect their plants. By priming plants with abiotic or biotic measures, managers can induce systemic acquired resistance (SAR) in plants to upregulate the ability to resist a pathogen. The accumulation of salicylic acid (SA) has been well researched and supported to be necessary for inducing SAR against pathogens. In previous research it has been shown that the functional analog of SA, acibenzolar S-methyl, has induced SAR and reduced disease severity. Acibenzolar S-methyl induces SAR when applied to plant foliage, but it does not have any antimicrobial activity to kill any pathogens on the foliage at the time of treatment. In previous research ozone has been successful at inducing SAR to reduce disease severity. Applying ozone as a treatment for greenhouse and nursery managers is not practical or safe since it is hazardous to the respiratory system. Chlorine dioxide is a powerful oxidant disinfectant that can be applied as a foliar spray to kill harmful pathogens, but it has not been reported whether it could induce plant defenses. This research study investigated whether a commercial formulation of chlorine dioxide [Electro-biocide® (E-B)] could be used as a foliar application to plants to induce SAR. E-B is a proprietary blend of ClO2, pH buffer, and a sarcosinate surfactant. There were a total of four spray treatments that were evaluated on plants inoculated with a bacterial wilt and on a set of non-inoculated plants. The light red kidney bean plants were treated with E-B at 200 mg l-1 ClO2, E-B 400 mg l-1 ClO2, acibenzolar S-methyl (Actigard™) and a water control to evaluate disease resistance when inoculated with Curtobacterium flaccumfaciens pv. flaccumfaciens. Treated plants were evaluated for both inoculated plants and non-inoculated plants. SA concentrations were measured five days after treatment and one day after inoculation. Leaf samples were collected to measure SA every three hours over the course of the day starting at 0700 hours and ending 2200 hours. A second SA measurement was taken at the end of the study 61 days after planting (44 days after treatment) to observe if there were any changes in SA level. Chlorophyll fluorescence measurements were taken to observe stress in response to the spray treatments and disease infection. Carbon dioxide (CO2) gas exchange measurements were taken to observe the vigor or decline within the spray treatments and infection status. At the end of the study plants were harvested for foliage, pod, stem dry weight, and leaf area. The first photosynthesis measurements on non-inoculated plants E-B 200 mg ClO2 l-1 and 400 mg l-1 ClO2 treatments declined, but recovered to control levels one week later. Inoculated plants treated with E-B and Actigard™ showed either the same or increased photosynthesis rates when compared to water. Chlorophyll fluorescence measurements indicated there was no stress due to the spray treatments. Five days after spray treatments the SA measurements showed that both concentrations of E-B resulted in an increase in SA accumulation. E-B 400 mg l-1 ClO2 caused the greatest SA response. E-B 400 mg l-1 ClO2 treated plant’s had a 15 fold increase in SA concentrations at its highest peak when compared to water. E-B 200 mg l-1 ClO2 had the second highest SA concentrations. It had a 5.9 fold increase at its highest peak when compared to water control plants. Actigard™ treated plants did not result in different SA concentrations from the water control plants. The SA concentrations levels at 44 days after treatment for all plants that were not inoculated returned to normal levels. SA levels for inoculated plants and all spray treatments continued to rise for the duration of the study. There were no differences in biomass measurements between spray treatments. All non-inoculated plants had a greater biomass measurements when compared to all the inoculated plants. These results conclude that E-B 200 mg l-1 ClO2 and E-B 400 mg l-1 ClO2 were able to prime plant defenses for SAR response. The rise in SA concentrations confirm that E-B was able to interact within the leaf as an elicitor for SAR. Unfortunately the biomass measurements for inoculated E-B treated plants did not show any difference from inoculated control plants. This indicates that the E-B treatment was not able to reduce the disease severity with CFF. Actigard (acibenzolar-S methyl) has been successful with inducing SAR and reducing disease severity in other studies. In this study Actigard was also unsuccessful in reducing disease severity. This indicates that CFF may have had too great of pressure for the inoculated plants to overcome. E-B should be investigated further with other pathogens.

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