A central role for<i>S</i>-nitrosothiols in plant disease resistance

DOI Web Site 被引用文献4件
  • Angela Feechan
    Institute of Molecular Plant Sciences, School of Biological Sciences, University of Edinburgh, King's Buildings, Edinburgh EH9 3JR, United Kingdom; and Trait Research, Syngenta, Jealott's Hill, Bracknell, Berkshire RG42 6EY, United Kingdom
  • Eunjung Kwon
    Institute of Molecular Plant Sciences, School of Biological Sciences, University of Edinburgh, King's Buildings, Edinburgh EH9 3JR, United Kingdom; and Trait Research, Syngenta, Jealott's Hill, Bracknell, Berkshire RG42 6EY, United Kingdom
  • Byung-Wook Yun
    Institute of Molecular Plant Sciences, School of Biological Sciences, University of Edinburgh, King's Buildings, Edinburgh EH9 3JR, United Kingdom; and Trait Research, Syngenta, Jealott's Hill, Bracknell, Berkshire RG42 6EY, United Kingdom
  • Yiqin Wang
    Institute of Molecular Plant Sciences, School of Biological Sciences, University of Edinburgh, King's Buildings, Edinburgh EH9 3JR, United Kingdom; and Trait Research, Syngenta, Jealott's Hill, Bracknell, Berkshire RG42 6EY, United Kingdom
  • Jacqueline A. Pallas
    Institute of Molecular Plant Sciences, School of Biological Sciences, University of Edinburgh, King's Buildings, Edinburgh EH9 3JR, United Kingdom; and Trait Research, Syngenta, Jealott's Hill, Bracknell, Berkshire RG42 6EY, United Kingdom
  • Gary J. Loake
    Institute of Molecular Plant Sciences, School of Biological Sciences, University of Edinburgh, King's Buildings, Edinburgh EH9 3JR, United Kingdom; and Trait Research, Syngenta, Jealott's Hill, Bracknell, Berkshire RG42 6EY, United Kingdom

抄録

<jats:p>Animal<jats:italic>S</jats:italic>-nitrosoglutathione reductase (GSNOR) governs the extent of cellular<jats:italic>S</jats:italic>-nitrosylation, a key redox-based posttranslational modification. Mutations in<jats:italic>AtGSNOR1</jats:italic>, an<jats:italic>Arabidopsis thaliana GSNOR</jats:italic>, modulate the extent of cellular<jats:italic>S</jats:italic>-nitrosothiol (SNO) formation in this model plant species. Loss of<jats:italic>AtGSNOR1</jats:italic>function increased SNO levels, disabling plant defense responses conferred by distinct resistance (<jats:italic>R</jats:italic>) gene subclasses. Furthermore, in the absence of<jats:italic>AtGSNOR1</jats:italic>, both basal and nonhost disease resistance are also compromised. Conversely, increased AtGSNOR1 activity reduced SNO formation, enhancing protection against ordinarily virulent microbial pathogens. Here we demonstrate that AtGSNOR1 positively regulates the signaling network controlled by the plant immune system activator, salicylic acid. This contrasts with the function of this enzyme in mice during endotoxic shock, where GSNOR antagonizes inflammatory responses. Our data imply SNO formation and turnover regulate multiple modes of plant disease resistance.</jats:p>

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