4.5 Article

Dissecting Contrasts in Cell Death, Hormone, and Defense Signaling in Response to Botrytis cinerea and Reactive Oxygen Species

Journal

MOLECULAR PLANT-MICROBE INTERACTIONS
Volume 34, Issue 1, Pages 75-87

Publisher

AMER PHYTOPATHOLOGICAL SOC
DOI: 10.1094/MPMI-07-20-0202-R

Keywords

cell death; defense signaling pathways; ethylene; fungus-plant interactions; jasmonic acid; salicylic acid

Funding

  1. Academy of Finland, Center of Excellence in the Molecular Biology of Primary Producers 2014-2019 [271832, 307335]
  2. Ella ja Georg Ehrnroothin Saatio grant
  3. University of Helsinki Doctoral Programme in Plant Sciences

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Plants require interaction between different signaling pathways, including hormones like ethylene, salicylic acid, and jasmonic acid, to respond to stress and deploy defenses. Reactive oxygen species also play a crucial role as signaling molecules in early defense responses. Research has shown that hormone signaling is important for plant resistance to pathogens, and the transcription factor SRI_ is identified as a key regulator of plant defensin expression and cell death.
Plants require interaction between signaling pathways to differentiate and integrate stress responses and deploy appropriate defenses. The hormones ethylene, salicylic acid (SA), and jasmonic acid (JA) are important regulators of plant defenses. Numerous interactions between these signaling pathways are the cornerstone of robust plant immunity. Additionally, during the early response to pathogens, reactive oxygen species (ROS) act as signaling molecules. Here, we examined the extent of signal interaction in the early stages of Botrytis cinerea infection. To enable a comparison between B. cinerea infection with ROS signaling, we subjected plants to ozone treatment, which stimulates an apoplastic ROS burst. We used a collection of single, double, and triple signaling mutants defective in hormone signaling and biosynthesis and subjected them to B. cinerea infection and ozone treatment at different timepoints. We examined lesion size, cell death, and gene expression (both quantitatively and spatially). The two treatments shared many similarities, especially in JA-insensitive mutants, which were sensitive to both treatments. Unexpectedly, a B. cinerea- susceptible JA-insensitive mutant (coil), became tolerant when both SA biosynthesis and signaling was impaired (coil npr1 sid2), demonstrating that JA responses may be under the control of SA. Extensive marker gene analysis indicated JA as the main regulator of both B. cinerea and ozone defenses. In addition, we identified the transcription factor SRI_ as a crucial regulator of PLANT DEFENSIN expression and cell-death regulation, which contributes to resistance to B. cinerea. Overall, our work further defines the context of ROS in plant defense signaling.

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