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DOI 10.1016/j.ecoenv.2017.09.011

Медицинская библиотека · Ecotoxicology and environmental safety · 2017

Enhanced Arabidopsis disease resistance against Botrytis cinerea induced by sulfur dioxide.

Xue Meizhao, Yi Huilan

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Аннотация

Sulfur dioxide (SO2) is a common air pollutant that has complex impacts on plants. The effect of prior exposure to 30mgm-3 SO2 on defence against Botrytis cinerea (B. cinerea) in Arabidopsis thaliana and the possible mechanisms of action were investigated. The results indicated that pre-exposure to 30mgm-3 SO2 resulted in significantly enhanced resistance to B. cinerea infection. SO2 pre-treatment significantly enhanced the activities of defence-related enzymes including phenylalanine ammonia-lyase (PAL), polyphenol oxidase (PPO), β-1,3-glucanase (BGL) and chitinase (CHI). Transcripts of the defence-related genes PAL, PPO, PR2, and PR3, encoding PAL, PPO, BGL and CHI, respectively, were markedly elevated in Arabidopsis plants pre-exposed to SO2 and subsequently inoculated with B. cinerea (SO2+ treatment group) compared with those that were only treated with SO2 (SO2) or inoculated with B. cinerea (CK+). Moreover, SO2 pre-exposure also led to significant increases in the expression levels of MIR393, MIR160 and MIR167 in Arabidopsis. Meanwhile, the expression of known targets involved in the auxin signalling pathway, was negatively correlated with their corresponding miRNAs. Additionally, the transcript levels of the primary auxin-response genes GH3-like, BDL/IAA12, and AXR3/IAA17 were markedly repressed. Our findings indicate that 30mgm-3 SO2 pre-exposure enhances disease resistance against B. cinerea in Arabidopsis by priming defence responses through enhancement of defence-related gene expression and enzyme activity, and miRNA-mediated suppression of the auxin signalling pathway.

Для цитирования: Xue Meizhao, Yi Huilan. Enhanced Arabidopsis disease resistance against Botrytis cinerea induced by sulfur dioxide.. Ecotoxicology and environmental safety. 2017. DOI: 10.1016/j.ecoenv.2017.09.011.

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