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

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dc.contributor.author Vuorinen, Katariina
dc.contributor.author Zamora, Olena
dc.contributor.author Vaahtera, Lauri
dc.contributor.author Overmyer, Kirk
dc.contributor.author Brosché, Mikael
dc.date.accessioned 2021-03-08T08:18:01Z
dc.date.available 2021-03-08T08:18:01Z
dc.date.issued 2021-01
dc.identifier.citation Vuorinen , K , Zamora , O , Vaahtera , L , Overmyer , K & Brosché , M 2021 , ' Dissecting Contrasts in Cell Death, Hormone, and Defense Signaling in Response to Botrytis cinerea and Reactive Oxygen Species ' , Molecular Plant - Microbe Interactions , vol. 34 , no. 1 , pp. 75-87 . https://doi.org/10.1094/MPMI-07-20-0202-R
dc.identifier.other PURE: 159816312
dc.identifier.other PURE UUID: a6efbba5-90c0-427e-b55d-cd3945d55e36
dc.identifier.other WOS: 000611544800007
dc.identifier.other ORCID: /0000-0002-7398-3453/work/90526473
dc.identifier.other ORCID: /0000-0002-1135-2496/work/90526831
dc.identifier.uri http://hdl.handle.net/10138/327613
dc.description.abstract 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. en
dc.format.extent 13
dc.language.iso eng
dc.relation.ispartof Molecular Plant - Microbe Interactions
dc.rights cc_by_nc_nd
dc.rights.uri info:eu-repo/semantics/openAccess
dc.subject ETHYLENE
dc.subject GROWTH
dc.subject JASMONIC ACID
dc.subject MUTANT
dc.subject PLANT DEFENSE
dc.subject PROTEIN
dc.subject REPRESSION
dc.subject RESISTANCE
dc.subject cell death
dc.subject defense signaling pathways
dc.subject ethylene
dc.subject fungus-plant interactions
dc.subject jasmonic acid
dc.subject salicylic acid
dc.subject 1182 Biochemistry, cell and molecular biology
dc.subject 11831 Plant biology
dc.title Dissecting Contrasts in Cell Death, Hormone, and Defense Signaling in Response to Botrytis cinerea and Reactive Oxygen Species en
dc.type Article
dc.contributor.organization Organismal and Evolutionary Biology Research Programme
dc.contributor.organization Faculty of Biological and Environmental Sciences
dc.contributor.organization Viikki Plant Science Centre (ViPS)
dc.contributor.organization Biosciences
dc.contributor.organization Plant-Fungal Interactions Group
dc.contributor.organization Plant stress and natural variation
dc.contributor.organization Plant Biology
dc.description.reviewstatus Peer reviewed
dc.relation.doi https://doi.org/10.1094/MPMI-07-20-0202-R
dc.relation.issn 0894-0282
dc.rights.accesslevel openAccess
dc.type.version publishedVersion

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