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dc.contributor.authorHunziker, Lukas
dc.contributor.authorTarallo, M.
dc.contributor.authorGough, K.
dc.contributor.authorGuo, M.
dc.contributor.authorHargreaves, C.
dc.contributor.authorLoo, T.S.
dc.contributor.authorMcDougal, R.L.
dc.contributor.authorMesarich, C.H.
dc.contributor.authorBradshaw, R.E.
dc.date.accessioned2024-08-08T06:01:15Z
dc.date.available2024-08-08T06:01:15Z
dc.date.issued2021
dc.identifier.citationHunziker, L. and Tarallo, M. and Gough, K. and Guo, M. and Hargreaves, C. and Loo, T.S. and McDougal, R.L. et al. 2021. Apoplastic effector candidates of a foliar forest pathogen trigger cell death in host and non-host plants. Scientific Reports. 11 (1): ARTN 19958.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/95662
dc.identifier.doi10.1038/s41598-021-99415-5
dc.description.abstract

Forests are under threat from pests, pathogens, and changing climate. A major forest pathogen worldwide is the hemibiotroph Dothistroma septosporum, which causes dothistroma needle blight (DNB) of pines. While D. septosporum uses effector proteins to facilitate host infection, it is currently unclear whether any of these effectors are recognised by immune receptors to activate the host immune system. Such information is needed to identify and select disease resistance against D. septosporum in pines. We predicted and investigated apoplastic D. septosporum candidate effectors (DsCEs) using bioinformatics and plant-based experiments. We discovered DsCEs that trigger cell death in the angiosperm Nicotiana spp., indicative of a hypersensitive defence response and suggesting their recognition by immune receptors in non-host plants. In a first for foliar forest pathogens, we developed a novel protein infiltration method to show that tissue-cultured pine shoots can respond with a cell death response to a DsCE, as well as to a reference cell death-inducing protein. The conservation of responses across plant taxa suggests that knowledge of pathogen–angiosperm interactions may also be relevant to pathogen–gymnosperm interactions. These results contribute to our understanding of forest pathogens and may ultimately provide clues to disease immunity in both commercial and natural forests.

dc.languageEnglish
dc.publisherNATURE PORTFOLIO
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectScience & Technology
dc.subjectMultidisciplinary Sciences
dc.subjectScience & Technology - Other Topics
dc.subjectDOTHISTROMA NEEDLE BLIGHT
dc.subjectCLADOSPORIUM-FULVUM
dc.subjectFUNGAL EFFECTORS
dc.subjectVIRULENCE FACTOR
dc.subjectRICH PROTEIN
dc.subjectRESISTANCE
dc.subjectRECOGNITION
dc.subjectGENE
dc.subjectELICITOR
dc.subjectIMMUNITY
dc.subjectAscomycota
dc.subjectCell Death
dc.subjectDisease Resistance
dc.subjectHost-Pathogen Interactions
dc.subjectPinus
dc.subjectPlant Diseases
dc.subjectNicotiana
dc.subjectAscomycota
dc.subjectPinus
dc.subjectCell Death
dc.subjectPlant Diseases
dc.subjectHost-Pathogen Interactions
dc.subjectDisease Resistance
dc.subjectNicotiana
dc.titleApoplastic effector candidates of a foliar forest pathogen trigger cell death in host and non-host plants
dc.typeJournal Article
dcterms.source.volume11
dcterms.source.number1
dcterms.source.issn2045-2322
dcterms.source.titleScientific Reports
dc.date.updated2024-08-08T06:00:59Z
curtin.departmentSchool of Molecular and Life Sciences (MLS)
curtin.accessStatusOpen access
curtin.facultyFaculty of Science and Engineering
curtin.contributor.orcidHunziker, Lukas [0000-0002-4678-6518]
curtin.identifier.article-numberARTN 19958
dcterms.source.eissn2045-2322
curtin.repositoryagreementV3


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