In the last decade, nitric oxide (NO) has been extensively studied in plants and is now well-recognized as a key signaling mediator during defense response to pathogens. In plants like in animals, NO acts directly or through mediators of its activity such as reactive NO derivatives (RNS), which can affect protein activity, and second messengers. In our laboratory we aim at deciphering the “signaling network” mediated in plant by NO and RNS upon pathogen attack. Using the specific dye HKGreen-2 in a photometric assay, we demonstrated that peroxynitrite, a RNS originated by the reaction between NO and O2-, accumulates in plants during the hypersensitive response (HR). This molecule, known as a toxic molecule in animals, is not a “death messenger” of NO in plants. Its accumulation in plants undergoing HR correlates with an increase in tyrosine nitrated proteins and in vitro peroxynitrite targets specifically some MAPK kinases, inhibiting their activity by tyrosine nitration. Together these results suggest a key role for peroxynitrite in fine-tuning cellular signaling in plant defense responses. Besides its effect on regulating plant cellular signaling, we found that NO can participate in plant defenses also by inhibiting pathogen effector activity. We identified the effector HopAI1, a phosphothreonine lyase produced by many P. syringae strains which suppresses plant immunity via MAPK inhibition, as a target of NO. The activity of HopAI1 is inhibited by S-nitrosylation in vitro and, whereas HopAI1 expressed in Arabidopsis thaliana does not affect the HR induced by the avirulent pathogen Pst AvrRpt2, the expression of the mutated form of HopAI1 on the unique Cys (HopAI1CS) strongly reduces hypersensitive cell death and plant resistance. This suggests that during the HR, NO produced in response to the avirulent pathogen is able to inhibit HopAI1 by S-nitrosylation to prevent pathogen virulence and allow defense signaling.

Nitric oxide modulates activity both of plant and pathogen proteins during plant-pathogen interaction

VANDELLE, Elodie Genevieve Germaine;BELLIN, Diana;DELLEDONNE, Massimo
2012

Abstract

In the last decade, nitric oxide (NO) has been extensively studied in plants and is now well-recognized as a key signaling mediator during defense response to pathogens. In plants like in animals, NO acts directly or through mediators of its activity such as reactive NO derivatives (RNS), which can affect protein activity, and second messengers. In our laboratory we aim at deciphering the “signaling network” mediated in plant by NO and RNS upon pathogen attack. Using the specific dye HKGreen-2 in a photometric assay, we demonstrated that peroxynitrite, a RNS originated by the reaction between NO and O2-, accumulates in plants during the hypersensitive response (HR). This molecule, known as a toxic molecule in animals, is not a “death messenger” of NO in plants. Its accumulation in plants undergoing HR correlates with an increase in tyrosine nitrated proteins and in vitro peroxynitrite targets specifically some MAPK kinases, inhibiting their activity by tyrosine nitration. Together these results suggest a key role for peroxynitrite in fine-tuning cellular signaling in plant defense responses. Besides its effect on regulating plant cellular signaling, we found that NO can participate in plant defenses also by inhibiting pathogen effector activity. We identified the effector HopAI1, a phosphothreonine lyase produced by many P. syringae strains which suppresses plant immunity via MAPK inhibition, as a target of NO. The activity of HopAI1 is inhibited by S-nitrosylation in vitro and, whereas HopAI1 expressed in Arabidopsis thaliana does not affect the HR induced by the avirulent pathogen Pst AvrRpt2, the expression of the mutated form of HopAI1 on the unique Cys (HopAI1CS) strongly reduces hypersensitive cell death and plant resistance. This suggests that during the HR, NO produced in response to the avirulent pathogen is able to inhibit HopAI1 by S-nitrosylation to prevent pathogen virulence and allow defense signaling.
pathogen effector; s-nitrosylation; plant resistance
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11562/478792
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