- Email: [email protected]
Uncovering the roles of S-nitrosothiols in plant disease resistance
S256
Abstracts / Comparative Biochemistry and Physiology, Part A 146 (2007) S255 – S266
under oxidative stress. S-nitrosylation abrogates PrxII E activities enhancing other NO derived protein modifications, such as tyrosine nitration. We conclude that NO regulates the effects of its own radicals through S-nitrosylation of crucial components of the antioxidant defense system that function as common triggers for ROS and NO mediated signaling events. doi:10.1016/j.cbpa.2007.01.642
P5.3 Uncovering the roles of S-nitrosothiols in plant disease resistance G. Loake, A. Feechan, W. Yun, Y. Wang, (University of Edinburgh) Animal S-nitrosoglutathione reductase (GSNOR) governs the extent of cellular S-nitrosylation, a key redox-based posttranslational modification. Mutations in AtGSNOR1, an Arabidopsis thaliana GSNOR, modulate the extent of cellular Snitrosothiol (SNO) formation in this model plant species. Loss of AtGSNOR1 function increased SNO levels, disabling plant defence responses conferred by distinct resistance (R) gene subclasses. Furthermore, in the absence of AtGSNOR1, both basal and non-host 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. doi:10.1016/j.cbpa.2007.01.643
P5.4 NO provides mainly avr-dependent inputs into cell death mechanisms associated with the hypersensitive response in tobacco
elicitation events; the first dependent on host recognition of pathogen-associated molecular patterns (PAMPs) and the second on cell death eliciting avirulence (avr) gene products also encoded by the pathogen. In contrast, NO generation was monophasic and, by ∼1 h following inoculation, continued at a constant level for at last 12 h. Inoculation of tobacco with a Psph hrp mutant where avr (but not PAMP) elicitation is abolished, resulted in the production of the first rise in H2O2 but negligible levels of NO. Reducing NO levels using inhibitors of nitric oxide generation affected only the avr-dependent H2O2 generation. Suppressing the oxidative burst had no observable effect on NO generation. These data suggest that NO provided primarily avr-dependent inputs into Psphelicited HR. Evidence will also be presented that NO–ROS interactions influence cell death and certain defence gene expression via peroxynitrite and OH generation. doi:10.1016/j.cbpa.2007.01.644
P5.5 Nitric oxide signalling in plants J. Durner, S. Sell, (National Research Center for Environment and Health, Germany) Although many studies have implicated nitric oxide (NO) as a key regulator for many different physiological processes in plants, less is known about how this molecule regulates these different events. As a readily diffusible free radical, NO reacts with a variety of intracellular and extracellular targets and can act as activator or inhibitor of enzymes, ion-channels or transcription factors as well as modulator of protein function. Because of its reactivity with transition metals NO can also bind to metal ions of heme groups, thereby activating soluble guanylate cyclase producing cyclic GMP. A NO-dependent cGMP signalling pathway has been proposed for plants. NO can also react with the thiol group of cysteine residues to form Snitrosothiols (S-nitrosylation). The majority of all NO-affected proteins seem to be regulated by S-nitrosylation making this type of protein modification a predominant mechanism in NOsignalling. Here we want to focus on this NO-dependent modification of cysteine residues, describing its chemistry/ formation, specificity, and physiological function in plants. doi:10.1016/j.cbpa.2007.01.645
L. Mur, P. Kenton, F. Harren, (University of Wales, Aberystwyth); L. Laarhoven, A. Smith, (University of Nijmegen) The hypersensitive response (HR) is a localised programmed cell death that can aid in neutralising infections by pathogens. H2O2 and NO are proposed elicitors of the HR and we have employed in planta assays to measure the production of both (Mur et al., 2005 Plant Cell and Environment. 6: 65–78; Mur et al., 2005; Plant Physiology 138: 1247–1258) during a HR elicited in tobacco by Pseudomonas syringae pathovar phaseolicola (Psph). As in other studies, the simultaneous generation of NO and H2O2 was noted. H2O2 generation adopted a biphasic pattern reflecting two
P5.6 Quantitative proteomics of Arabidopsis plants submitted to oxidative stress L. Bindschedler, M. Palmblad, R. Cramer, (Universtiy of Reading) Reactive oxygen species are produced in plants responding to various biotic and abiotic stresses. Thus hydroponically grown Arabidopsis thaliana plants were treated with hydrogen
Abstracts / Comparative Biochemistry and Physiology, Part A 146 (2007) S255 – S266
under oxidative stress. S-nitrosylation abrogates PrxII E activities enhancing other NO derived protein modifications, such as tyrosine nitration. We conclude that NO regulates the effects of its own radicals through S-nitrosylation of crucial components of the antioxidant defense system that function as common triggers for ROS and NO mediated signaling events. doi:10.1016/j.cbpa.2007.01.642
P5.3 Uncovering the roles of S-nitrosothiols in plant disease resistance G. Loake, A. Feechan, W. Yun, Y. Wang, (University of Edinburgh) Animal S-nitrosoglutathione reductase (GSNOR) governs the extent of cellular S-nitrosylation, a key redox-based posttranslational modification. Mutations in AtGSNOR1, an Arabidopsis thaliana GSNOR, modulate the extent of cellular Snitrosothiol (SNO) formation in this model plant species. Loss of AtGSNOR1 function increased SNO levels, disabling plant defence responses conferred by distinct resistance (R) gene subclasses. Furthermore, in the absence of AtGSNOR1, both basal and non-host 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. doi:10.1016/j.cbpa.2007.01.643
P5.4 NO provides mainly avr-dependent inputs into cell death mechanisms associated with the hypersensitive response in tobacco
elicitation events; the first dependent on host recognition of pathogen-associated molecular patterns (PAMPs) and the second on cell death eliciting avirulence (avr) gene products also encoded by the pathogen. In contrast, NO generation was monophasic and, by ∼1 h following inoculation, continued at a constant level for at last 12 h. Inoculation of tobacco with a Psph hrp mutant where avr (but not PAMP) elicitation is abolished, resulted in the production of the first rise in H2O2 but negligible levels of NO. Reducing NO levels using inhibitors of nitric oxide generation affected only the avr-dependent H2O2 generation. Suppressing the oxidative burst had no observable effect on NO generation. These data suggest that NO provided primarily avr-dependent inputs into Psphelicited HR. Evidence will also be presented that NO–ROS interactions influence cell death and certain defence gene expression via peroxynitrite and OH generation. doi:10.1016/j.cbpa.2007.01.644
P5.5 Nitric oxide signalling in plants J. Durner, S. Sell, (National Research Center for Environment and Health, Germany) Although many studies have implicated nitric oxide (NO) as a key regulator for many different physiological processes in plants, less is known about how this molecule regulates these different events. As a readily diffusible free radical, NO reacts with a variety of intracellular and extracellular targets and can act as activator or inhibitor of enzymes, ion-channels or transcription factors as well as modulator of protein function. Because of its reactivity with transition metals NO can also bind to metal ions of heme groups, thereby activating soluble guanylate cyclase producing cyclic GMP. A NO-dependent cGMP signalling pathway has been proposed for plants. NO can also react with the thiol group of cysteine residues to form Snitrosothiols (S-nitrosylation). The majority of all NO-affected proteins seem to be regulated by S-nitrosylation making this type of protein modification a predominant mechanism in NOsignalling. Here we want to focus on this NO-dependent modification of cysteine residues, describing its chemistry/ formation, specificity, and physiological function in plants. doi:10.1016/j.cbpa.2007.01.645
L. Mur, P. Kenton, F. Harren, (University of Wales, Aberystwyth); L. Laarhoven, A. Smith, (University of Nijmegen) The hypersensitive response (HR) is a localised programmed cell death that can aid in neutralising infections by pathogens. H2O2 and NO are proposed elicitors of the HR and we have employed in planta assays to measure the production of both (Mur et al., 2005 Plant Cell and Environment. 6: 65–78; Mur et al., 2005; Plant Physiology 138: 1247–1258) during a HR elicited in tobacco by Pseudomonas syringae pathovar phaseolicola (Psph). As in other studies, the simultaneous generation of NO and H2O2 was noted. H2O2 generation adopted a biphasic pattern reflecting two
P5.6 Quantitative proteomics of Arabidopsis plants submitted to oxidative stress L. Bindschedler, M. Palmblad, R. Cramer, (Universtiy of Reading) Reactive oxygen species are produced in plants responding to various biotic and abiotic stresses. Thus hydroponically grown Arabidopsis thaliana plants were treated with hydrogen