Apoplastic effector candidates of a foliar forest pathogen trigger cell death in host and non-host plants

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 current...

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Main Authors: Lukas Hunziker, Mariana Tarallo, Keiko Gough, Melissa Guo, Cathy Hargreaves, Trevor S. Loo, Rebecca L. McDougal, Carl H. Mesarich, Rosie E. Bradshaw
Format: Article
Language:English
Published: Nature Publishing Group 2021-10-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-021-99415-5
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spelling doaj-0ca29a47e8fa404da18d6849a8ab117f2021-10-10T11:30:08ZengNature Publishing GroupScientific Reports2045-23222021-10-0111111210.1038/s41598-021-99415-5Apoplastic effector candidates of a foliar forest pathogen trigger cell death in host and non-host plantsLukas Hunziker0Mariana Tarallo1Keiko Gough2Melissa Guo3Cathy Hargreaves4Trevor S. Loo5Rebecca L. McDougal6Carl H. Mesarich7Rosie E. Bradshaw8Centre for Crop and Disease Management, Curtin UniversityBio-Protection Research Centre, School of Fundamental Sciences, Massey UniversityScion, New Zealand Forest Research Institute LtdBio-Protection Research Centre, School of Fundamental Sciences, Massey UniversityScion, New Zealand Forest Research Institute LtdBio-Protection Research Centre, School of Fundamental Sciences, Massey UniversityScion, New Zealand Forest Research Institute LtdBio-Protection Research Centre, School of Agriculture and Environment, Massey UniversityBio-Protection Research Centre, School of Fundamental Sciences, Massey UniversityAbstract 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.https://doi.org/10.1038/s41598-021-99415-5
collection DOAJ
language English
format Article
sources DOAJ
author Lukas Hunziker
Mariana Tarallo
Keiko Gough
Melissa Guo
Cathy Hargreaves
Trevor S. Loo
Rebecca L. McDougal
Carl H. Mesarich
Rosie E. Bradshaw
spellingShingle Lukas Hunziker
Mariana Tarallo
Keiko Gough
Melissa Guo
Cathy Hargreaves
Trevor S. Loo
Rebecca L. McDougal
Carl H. Mesarich
Rosie E. Bradshaw
Apoplastic effector candidates of a foliar forest pathogen trigger cell death in host and non-host plants
Scientific Reports
author_facet Lukas Hunziker
Mariana Tarallo
Keiko Gough
Melissa Guo
Cathy Hargreaves
Trevor S. Loo
Rebecca L. McDougal
Carl H. Mesarich
Rosie E. Bradshaw
author_sort Lukas Hunziker
title Apoplastic effector candidates of a foliar forest pathogen trigger cell death in host and non-host plants
title_short Apoplastic effector candidates of a foliar forest pathogen trigger cell death in host and non-host plants
title_full Apoplastic effector candidates of a foliar forest pathogen trigger cell death in host and non-host plants
title_fullStr Apoplastic effector candidates of a foliar forest pathogen trigger cell death in host and non-host plants
title_full_unstemmed Apoplastic effector candidates of a foliar forest pathogen trigger cell death in host and non-host plants
title_sort apoplastic effector candidates of a foliar forest pathogen trigger cell death in host and non-host plants
publisher Nature Publishing Group
series Scientific Reports
issn 2045-2322
publishDate 2021-10-01
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.
url https://doi.org/10.1038/s41598-021-99415-5
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