ABA Suppresses Botrytis cinerea Elicited NO Production in Tomato to Influence H2O2 Generation and Increase Host Susceptibility.

Anushen Sivakumaran,Anushen Sivakumaran,Julian Mandon,Julian Mandon,Aderemi Akinyemi,Julian Mandon,Michael A Hall,Frans J M Harren,Michael A Hall,Luis A J Mur,Luis A J Mur,Simona M Cristescu,Simona M Cristescu,Simona M Cristescu,Aderemi Akinyemi

doi:10.3389/fpls.2016.00709

Abstract

Abscisic acid (ABA) production has emerged a susceptibility factor in plant-pathogen interactions. This work examined the interaction of ABA with nitric oxide (NO) in tomato following challenge with the ABA-synthesizing pathogen, Botrytis cinerea. Trace gas detection using a quantum cascade laser detected NO production within minutes of challenge with B. cinerea whilst photoacoustic laser detection detected ethylene production – an established mediator of defense against this pathogen – occurring after 6 h. Application of the NO generation inhibitor N-Nitro-L-arginine methyl ester (L-NAME) suppressed both NO and ethylene production and resistance against B. cinerea. The tomato mutant sitiens fails to accumulate ABA, shows increased resistance to B. cinerea and we noted exhibited elevated NO and ethylene production. Exogenous application of L-NAME or ABA reduced NO production in sitiens and reduced resistance to B. cinerea. Increased resistance to B. cinerea in sitiens have previously been linked to increased reactive oxygen species (ROS) generation but this was reduced in both L-NAME and ABA-treated sitiens. Taken together, our data suggests that ABA can decreases resistance to B. cinerea via reduction of NO production which also suppresses both ROS and ethylene production.

Highlights

The outcome of pathogen interactions with plants is governed by multiple events
We have demonstrated that Nitric oxide (NO) contributes both to ethylene production and resistance to B. cinerea in Arabidopsis (Mur et al, 2012)
To investigate the role of NO in tomato challenged with B. cinerea, the production of NO was measured using a QCLbased approach (Figure 1A)

Summary

Introduction

The outcome of pathogen interactions with plants is governed by multiple events (reviewed by Jones and Dangl, 2006). Pathogens have evolved a range of effectors which can suppress PTI, some of which may be recognized by the host–classically by Resistance (R) genes – to initiate effector-triggered immunity (ETI) which can lead to the form of programmed cell death known as the hypersensitive response (HR; Mur et al, 2008). Superimposed on these interactions are the various pathogen-derived toxins, enzymes, and host modifying proteins that can drive symptom development. Such examples demonstrate the close interactive role of NO with other signaling pathways which include JA and Et (Mur et al, 2013)

Methods

Results

Conclusion