Analysis of the Plant bos1 Mutant Highlights Necrosis as an Efficient Defence Mechanism during D. dadantii/Arabidospis thaliana Interaction

Abstract

Dickeya dadantii is a broad host range phytopathogenic bacterium provoking soft rot disease on many plants including Arabidopsis. We showed that, after D. dadantii infection, the expression of the Arabidopsis BOS1 gene was specifically induced by the production of the bacterial PelB/C pectinases able to degrade pectin. This prompted us to analyze the interaction between the bos1 mutant and D. dadantii. The phenotype of the infected bos1 mutant is complex. Indeed, maceration symptoms occurred more rapidly in the bos1 mutant than in the wild type parent but at a later stage of infection, a necrosis developed around the inoculation site that provoked a halt in the progression of the maceration. This necrosis became systemic and spread throughout the whole plant, a phenotype reminiscent of that observed in some lesion mimic mutants. In accordance with the progression of maceration symptoms, bacterial population began to grow more rapidly in the bos1 mutant than in the wild type plant but, when necrosis appeared in the bos1 mutant, a reduction in bacterial population was observed. From the plant side, this complex interaction between D. dadantii and its host includes an early plant defence response that comprises reactive oxygen species (ROS) production accompanied by the reinforcement of the plant cell wall by protein cross-linking. At later timepoints, another plant defence is raised by the death of the plant cells surrounding the inoculation site. This plant cell death appears to constitute an efficient defence mechanism induced by D. dadantii during Arabidopsis infection.

NAD Acts as an Integral Regulator of Multiple Defense Layers

“…Surprisingly, our pathogenicity assays clearly showed that NAD-induced defense is effective against a range of pathogens with different lifestyles (Fig. 1), including the avirulent hemibiotrophic pathogen Pst-AvrRpt2 and the virulent hemibiotrophic pathogen D. dadantii (which are resisted by SA-and ROSrelated defenses; Katagiri et al, 2002;Fagard et al, 2007;Kraepiel et al, 2011) as well as the necrotrophic pathogen B. cinerea (which is sensitive to JA-dependent defenses; Glazebrook, 2005). Our metabolomics analysis has demonstrated that exogenously applied NAD and intracellular accumulation of NAD simultaneously increased pools of SA, JA, and ABA (Table I; Supplemental Fig.…”

Modifications of sphingolipid content affect tolerance to hemibiotrophic and necrotrophic pathogens by modulating plant defense responses in Arabidopsis

“…8). Several studies demonstrated that resistance against B. cinerea (and other necrotrophs) is accompanied by the generation of ROS, and mutants impaired in ROS production failed to resist the necrotrophic pathogen (Contreras-Cornejo et al, 2011;Kraepiel et al, 2011;L'Haridon et al, 2011;Rasul et al, 2012;Savatin et al, 2014;Zhang et al, 2014). It has been shown that LCBs but not LCB-Ps alone are able to induce ROS production (Peer et al, 2011).…”

Manipulation of ABA Content in Arabidopsis thaliana Modifies Sensitivity and Oxidative Stress Response to Dickeya dadantii and Influences Peroxidase Activity

“…Aerial plant tissues were collected at different time points post-inoculation and ground in liquid nitrogen to a fine powder. This infection procedure, close to a natural leaf infection by splashing, was compatible with short studies of infection rate and avoided wound-related transcriptional responses (Kraepiel et al, 2011). …”

“…Dickeya dadantii strains used in this study derived from the 3937 wild type (WT) strain and were previously described (Kraepiel et al, 2011). The secretion mutants prtE , outC , and hrcC are respectively impaired in the type I, type II, and type III protein secretion systems.…”

“…Induction of JA and SA pathways (Fagard et al, 2007), iron transport and storage (Dellagi et al, 2005, 2009) and ROS production associated with cell wall protein cross-linking (Fagard et al, 2007; Asselbergh et al, 2008a; Kraepiel et al, 2011) have been demonstrated. We have also shown that the bacterium induces necrosis around the maceration zone in Arabidopsis leaves, which can stop disease progression (Kraepiel et al, 2011), highlighting the importance of bacterial spread into healthy tissues before the symptoms appear. Phenotypic analyses of plant mutants have, however, shown that in most cases disruption of a single defense reaction has only a weak, if any, effect on disease development.…”