Nitric oxide and S-nitrosoglutathione function additively during plant immunity

© 2016 The Authors. New Phytologist © 2016 New Phytologist Trust.

Bibliographische Detailangaben
Veröffentlicht in:The New phytologist. - 1979. - 211(2016), 2 vom: 15. Juli, Seite 516-26
1. Verfasser: Yun, Byung-Wook (VerfasserIn)
Weitere Verfasser: Skelly, Michael J, Yin, Minghui, Yu, Manda, Mun, Bong-Gyu, Lee, Sang-Uk, Hussain, Adil, Spoel, Steven H, Loake, Gary J
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2016
Zugriff auf das übergeordnete Werk:The New phytologist
Schlagworte:Journal Article S-nitrosylation and S-nitrosothiols hypersensitive response nitric oxide (NO) plant disease resistance plant immunity post-translational modifications redox signalling Arabidopsis Proteins Nitric Oxide mehr... 31C4KY9ESH S-Nitrosoglutathione 57564-91-7
Beschreibung
Zusammenfassung:© 2016 The Authors. New Phytologist © 2016 New Phytologist Trust.
Nitric oxide (NO) is emerging as a key regulator of diverse plant cellular processes. A major route for the transfer of NO bioactivity is S-nitrosylation, the addition of an NO moiety to a protein cysteine thiol forming an S-nitrosothiol (SNO). Total cellular levels of protein S-nitrosylation are controlled predominantly by S-nitrosoglutathione reductase 1 (GSNOR1) which turns over the natural NO donor, S-nitrosoglutathione (GSNO). In the absence of GSNOR1 function, GSNO accumulates, leading to dysregulation of total cellular S-nitrosylation. Here we show that endogenous NO accumulation in Arabidopsis, resulting from loss-of-function mutations in NO Overexpression 1 (NOX1), led to disabled Resistance (R) gene-mediated protection, basal resistance and defence against nonadapted pathogens. In nox1 plants both salicylic acid (SA) synthesis and signalling were suppressed, reducing SA-dependent defence gene expression. Significantly, expression of a GSNOR1 transgene complemented the SNO-dependent phenotypes of paraquat resistant 2-1 (par2-1) plants but not the NO-related characters of the nox1-1 line. Furthermore, atgsnor1-3 nox1-1 double mutants supported greater bacterial titres than either of the corresponding single mutants. Our findings imply that GSNO and NO, two pivotal redox signalling molecules, exhibit additive functions and, by extension, may have distinct or overlapping molecular targets during both immunity and development
Beschreibung:Date Completed 31.01.2018
Date Revised 16.03.2022
published: Print-Electronic
Citation Status MEDLINE
ISSN:1469-8137
DOI:10.1111/nph.13903