• 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • br GSNOR regulates SA synthesis and SA signalling


    GSNOR1 regulates SA synthesis and SA signalling The phenolic metabolite salicylic A-674563 (SA) is a powerful immune activator in plants. Moreover, mutations that disable SA biosynthesis or transgenes that result in its depletion compromise both resistance (R) gene-mediated and basal resistance, leading to enhanced disease susceptibility towards biotrophic and hemi-biotrophic pathogens [37], [38], [39]. The loss-of-function mutant atgsnor1-3 in Arabidopsis increases cellular GSNO levels and leads to a striking reduction in SA accumulation [33] (Fig. 1). These findings could be explained by either reduced SA synthesis or increased SA turnover. However, as the amount of O-β-glucoside (SAG), a less toxic storage form of SA, is also depleted in atgsnor1-3 plants, this data implies that SA levels are low in this line due to decreased SA synthesis [33]. In support, our recent data suggest that increasing GSNO concentrations resulting from loss of GSNOR1 function impacts SA synthesis. Further, this reduction in SA production appears to be mediated at the level of transcription. Thus, rising GSNO concentrations negatively regulate the expression of genes encoding enzymes integral to the generation of SA [Keyani et al. unpublished data]. In contrast, an earlier study showed that exogenous application of NO donors to tobacco plants significantly increased SA accumulation and PR1 gene expression [9]. Further, exogenous NO treatment has also been reported to induce systemic acquired resistance (SAR) in tobacco plants but not in transgenic lines that were compromised in SA accrual [40]. The discrepancy between these results may reflect the location of SNO/NO accumulation: intracellular compared to apoplastic. Alternatively, perhaps SNO and NO mediate different responses. In addition to mediating S-nitrosylation, NO can also become covalently bound to transition metals as heme-NO or dinitrosyl non-heme iron complexes [31]. Therefore, while many might overlap, some cellular responses cued in reaction to NO may be distinct from those triggered by GSNO accumulation. The emerging evidence suggests that the absence of GSNOR1 activity also disables SA signalling, in addition to SA synthesis. Thus, exogenous SA application to atgsnor1-3 plants results in delayed and weak activation of SA-dependent defence genes [33]. The mechanisms by which increased levels of GSNO and protein SNO blunt SA signalling are just beginning to be uncovered (see next section). Hence, GSNOR1 function regulates both SA synthesis and SA signalling and thereby controls the activity of at least two nodes embedded within the SA signal pathway.
    GSNOR1 regulates plant disease resistance As SA is such a fundamental immune activator in plants and its synthesis and signalling is governed by GSNOR1, modulation of this enzyme activity would be expected to affect the development of plant disease resistance. Indeed, in the absence of GSNOR1 function Arabidopsis plants have been shown to be disabled in R gene-mediated protection mediated by either the Toll interleukin (TOLL) or coiled-coiled class of nucleotide binding site leucine rich repeat (NBS-LRR) proteins, which possess different signalling requirements [1]. Furthermore, atgsnor1-3 plants are compromised in basal resistance against the bacterial pathogen Pseudomonas syringae pv. tomato (Pst) DC3000 and the oomycete, Hyaloperonospora arabidopsidis. Plants are protected against the vast majority of potential pathogens due to a phenomenon termed non-host resistance (NHR). However, the underlying molecular mechanisms of this multi-factorial trait are not well understood. In the absence of GSNOR1 function Arabidopsis plants support the growth of the wheat powdery mildew pathogen, Blumeria graminis f.sp. tritici. This fungus is a major pathogen of wheat but is not adapted for growth on Arabidopsis. Moreover, atgsnor1-3 plants also become hosts for Pseudomonas syringae pv. phaseolicola and Pseudomonas fluorescens. Wild-type Arabidopsis plants do not support the growth of these non-adapted bacterial pathogens. Thus, GSNOR1 also governs the development of NHR against both fungal and bacterial pathogens [33]. Collectively, these data imply that GSNOR1 controls multiple modes of plant disease resistance.