The AtrbohD-Mediated Oxidative Burst Elicited by Oligogalacturonides in Arabidopsis Is Dispensable for the Activation of Defense Responses Effective against Botrytis cinerea    

Abstract

Oligogalacturonides (OGs) are endogenous elicitors of defense responses released after partial degradation of pectin in the plant cell wall. We have previously shown that, in Arabidopsis (Arabidopsis thaliana), OGs induce the expression of PHYTOALEXIN DEFICIENT3 (PAD3) and increase resistance to the necrotrophic fungal pathogen Botrytis cinerea independently of signaling pathways mediated by jasmonate, salicylic acid, and ethylene. Here, we illustrate that the rapid induction of the expression of a variety of genes by OGs is also independent of salicylic acid, ethylene, and jasmonate. OGs elicit a robust extracellular oxidative burst that is generated by the NADPH oxidase AtrbohD. This burst is not required for the expression of OG-responsive genes or for OG-induced resistance to B. cinerea, whereas callose accumulation requires a functional AtrbohD. OG-induced resistance to B. cinerea is also unaffected in powdery mildew resistant4, despite the fact that callose accumulation was almost abolished in this mutant. These results indicate that the OG-induced oxidative burst is not required for the activation of defense responses effective against B. cinerea, leaving open the question of the role of reactive oxygen species in elicitormediated defense.

Dual Roles of Reactive Oxygen Species and NADPH Oxidase RBOHD in an Arabidopsis-Alternaria Pathosystem

“…The latter was also found to be more significant than RBOHF as a source of Erwinia chrysanthemi-elicited ROS production and as a suppressor of E. chrysanthemiinduced soft rot in Arabidopsis (Fagard et al, 2007). Interestingly, AtrbohD knockout plants inoculated with another necrotrophic fungus, Botrytis cinerea, did not exhibit altered cell death response in comparison with wild-type plants (Torres et al, 2005;Galletti et al, 2008), which observation may indicate remarkable differences between fungal species that are normally considered similar as a result of their lifestyles.…”

“…(4) Lesion-free leaves of the hrl1 lesion-mimic mutant exhibit higher transcriptional rbohD induction than leaves actually displaying lesions (Devadas et al, 2002). (5) Most interestingly, as has been pointed out in two recent papers, pathogen-or host-associated molecular pattern elicitors such as flagellin (flg22) or oligogalacturonides do induce a rapid, transient, RBOHDdependent oxidative burst in Arabidopsis leaves detected by chemiluminescence or xylenol orange methods (Zhang et al, 2007;Galletti et al, 2008). When we reproduced flg22 treatment as described by Zhang et al (2007), DAB staining in our hands was not sensitive enough to detect this ROS response, which may indicate that early ROS accumulation occurs in a lower concentration range (M. Pogány and J. Durner, unpublished data).…”

“…We conclude from this result that active RBOHD negatively regulates the transcription of a limited number of genes and that this regulatory function is rather quantitative. In a recent work, RBOHD-derived ROS accumulation was excluded as an important regulator of oligogalacturonide-induced transcriptional responses in Arabidopsis (Galletti et al, 2008).…”

Reactive oxygen species and plant resistance to fungal pathogens

“…The treatment of Arabidopsis leaves with oligogalacturonides (OGs) elicits an AtRbohD-dependent oxidative burst and protects Arabidopsis plants from subsequent attack by B. cinerea. Despite the loss of the OG-elicited ROS-burst, atrbohD T-DNA mutants still exhibit an induction of defence genes and an increased resistance towards B. cinerea after OG-treatment (Galletti et al, 2008). A recent study suggests nitric oxide (NO) to act as an upstream regulator of the OG-elicited oxidative burst mediated by AtRbohD (Rasul et al, 2012).…”

The Arabidopsis NUCLEUS- AND PHRAGMOPLAST-LOCALIZED KINASE1-Related Protein Kinases Are Required for Elicitor-Induced Oxidative Burst and Immunity

“…An overlap but also some distinctive features exist between responses induced by PAMPs and DAMPs. For example, flg22 and OGs generate an extracellular oxidative burst mediated by RESPIRATORY BURST OXIDASE HOMOLOG D (RbohD) and induce protection against the necrotrophic fungus Botrytis cinerea independently of the ethylene, jasmonic acid, and salicylic acid pathways and of the RbohD-mediated production of reactive oxygen species (ROS; Zhang et al, 2007;Galletti et al, 2008). The inhibition of auxin responses is another feature shared by PAMPs and DAMPs (Savatin et al, 2011); in the case of OGs, the inhibition of auxin responses has been described as a true antagonism (Branca et al, 1988;Bellincampi et al, 1993;Savatin et al, 2011).…”