An Arabidopsis downy mildew non-RxLR effector suppresses induced plant cell death to promote biotroph infection.
Identifieur interne : 000306 ( Main/Exploration ); précédent : 000305; suivant : 000307An Arabidopsis downy mildew non-RxLR effector suppresses induced plant cell death to promote biotroph infection.
Auteurs : Florian Dunker [Allemagne] ; Lorenz Oberkofler [Allemagne] ; Bernhard Lederer [Allemagne] ; Adriana Trutzenberg [Allemagne] ; Arne Weiberg [Allemagne]Source :
- Journal of experimental botany [ 1460-2431 ] ; 2020.
Abstract
Our understanding of obligate biotrophic pathogens is limited by the scarce knowledge concerning the molecular function of virulence factors. We established Arabidopsis thaliana host induced gene silencing (HIGS) to explore gene functions of Hyaloperonospora arabidopsidis, including the CYSTEINE-RICH PROTEIN (HaCR)1, a potential secreted effector gene of this obligate biotrophic pathogen. HaCR1 HIGS resulted in H. arabidopsidis-induced local plant cell death and reduced pathogen reproduction. We functionally characterized HaCR1 by ectopic expression in Nicotiana benthamiana. HaCR1 was capable of inhibiting effector-triggered plant cell death. In consistence, HaCR1 expression in N. benthamiana led to stronger disease symptoms caused by the hemibiotrophic oomycete pathogen Phytophthora capsici, but reduced disease symptoms caused by the necrotrophic fungal pathogen Botrytis cinerea. Expressing HaCR1 in transgenic A. thaliana confirmed higher susceptibility to H. arabidopsidis and to the bacterial hemibiotrophic pathogen Pseudomonas syringae. Increased H. arabidopsidis infection was in accordance with reduced PATHOGENESIS RELATED (PR)1 induction. Expression of full-length HaCR1 was required for its function that was lost if the signal peptide was deleted, suggesting its site of action in the plant apoplast. This study provides phytopathological and molecular evidence for the importance of the widely spread, but largely unexplored class of non-RxLR effectors in biotrophic oomycetes.
DOI: 10.1093/jxb/eraa472
PubMed: 33063828
Affiliations:
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<front><div type="abstract" xml:lang="en">Our understanding of obligate biotrophic pathogens is limited by the scarce knowledge concerning the molecular function of virulence factors. We established Arabidopsis thaliana host induced gene silencing (HIGS) to explore gene functions of Hyaloperonospora arabidopsidis, including the CYSTEINE-RICH PROTEIN (HaCR)1, a potential secreted effector gene of this obligate biotrophic pathogen. HaCR1 HIGS resulted in H. arabidopsidis-induced local plant cell death and reduced pathogen reproduction. We functionally characterized HaCR1 by ectopic expression in Nicotiana benthamiana. HaCR1 was capable of inhibiting effector-triggered plant cell death. In consistence, HaCR1 expression in N. benthamiana led to stronger disease symptoms caused by the hemibiotrophic oomycete pathogen Phytophthora capsici, but reduced disease symptoms caused by the necrotrophic fungal pathogen Botrytis cinerea. Expressing HaCR1 in transgenic A. thaliana confirmed higher susceptibility to H. arabidopsidis and to the bacterial hemibiotrophic pathogen Pseudomonas syringae. Increased H. arabidopsidis infection was in accordance with reduced PATHOGENESIS RELATED (PR)1 induction. Expression of full-length HaCR1 was required for its function that was lost if the signal peptide was deleted, suggesting its site of action in the plant apoplast. This study provides phytopathological and molecular evidence for the importance of the widely spread, but largely unexplored class of non-RxLR effectors in biotrophic oomycetes.</div>
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<Abstract><AbstractText>Our understanding of obligate biotrophic pathogens is limited by the scarce knowledge concerning the molecular function of virulence factors. We established Arabidopsis thaliana host induced gene silencing (HIGS) to explore gene functions of Hyaloperonospora arabidopsidis, including the CYSTEINE-RICH PROTEIN (HaCR)1, a potential secreted effector gene of this obligate biotrophic pathogen. HaCR1 HIGS resulted in H. arabidopsidis-induced local plant cell death and reduced pathogen reproduction. We functionally characterized HaCR1 by ectopic expression in Nicotiana benthamiana. HaCR1 was capable of inhibiting effector-triggered plant cell death. In consistence, HaCR1 expression in N. benthamiana led to stronger disease symptoms caused by the hemibiotrophic oomycete pathogen Phytophthora capsici, but reduced disease symptoms caused by the necrotrophic fungal pathogen Botrytis cinerea. Expressing HaCR1 in transgenic A. thaliana confirmed higher susceptibility to H. arabidopsidis and to the bacterial hemibiotrophic pathogen Pseudomonas syringae. Increased H. arabidopsidis infection was in accordance with reduced PATHOGENESIS RELATED (PR)1 induction. Expression of full-length HaCR1 was required for its function that was lost if the signal peptide was deleted, suggesting its site of action in the plant apoplast. This study provides phytopathological and molecular evidence for the importance of the widely spread, but largely unexplored class of non-RxLR effectors in biotrophic oomycetes.</AbstractText>
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