Erwinia amylovora type three-secreted proteins trigger cell death and defense responses in Arabidopsis thaliana

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Mechanisms involved in fire blight protection of apple with an hrpL mutant of Erwinia amylovora

International audiencehrpL and hrpS mutants of Erwinia amylovora have been shown to be significantly more effective than hrp secretory mutants in preventing apple seedlings and apple flowers from developping fire blight symptoms caused by a virulent strain. Mechanisms involved in the protective effect obtained with an hrpL mutant were investigated. Two histochemical techniques (a two-step staining and an immunostaining technique) indicated that when simultaneously inoculated, cells of the two strains localized mainly in separate areas of the leaf tissues. In addition, leaves infiltrated with the hrpL mutant exibited a significant increase in peroxidase activity in contrast to an hrp secretion mutant. Mechanisms of the protective effect obtained with the hrpL mutant are proposed

DspA/E, a type III effector essential for Erwinia amylovora pathogenicity and growth in planta, induces cell death in host apple and nonhost tobacco plants

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Protection of apple against fire blight induced by an hrpL mutant of Erwinia amylovora

Correspondance : [email protected] audienceA regulatory hrpL non-virulent mutant of Erwinia amylovora is effective in controlling fire blight disease when inoculated on apple seedlings simultaneously with the pathogenic parental strain. Mechanisms involved in this protective effect were investigated. The use of two marker genes, uidA and lacZ, expressed in the hrpL mutant and the pathogenic strain, respectively, allowed to localize simultaneously the two inoculated strains in plant tissue. An anti-beta-glucuronidase antibody was also used to detect the hrpL mutant. Both techniques indicated that the two strains localized mainly in separate areas of the leaf tissue. In addition, leaves infiltrated with the hrpL mutant exhibited a significant increase in peroxidase activity in contrast to a hrp secretion mutant known to be less effective in the protection. It is suggested that protection obtained with the hrpL mutant relies on the physical separation between the mutant and the parental strain after co-inoculation and the rapid and sustained activation of plant defense mechanisms in reactive tissue, i.e. not invaded by the virulent strain

Molecular Nutrition and Epigenetics

Molecular nutrition is relatively recent research discipline that aims to decipher molecular effects of nutrition at the cellular level and identify mechanisms underlying potential impact on health, protective or deleterious. The development and the use of holistic “omics” approach in the last decade or two have revealed the complexity of action of different nutrients at the molecular level. These nutrigenomic studies have shown that nutrients can impact transcriptional and post transcriptional regulation of gene expression, by impacting expression of mRNA, non-coding RNAs (both short and long) and proteins, but also modulate epigenetic profile of the cells. The capacity of nutrients to exert these nutrigenomic effects can be related to the their ability to bind to cell signaling proteins, modulate their activity and consequently that of transcription factors. The feature article gives a rapid overview of molecular mechanisms impacted by different nutrients

Dickeya dadantii pectic enzymes necessary for virulence are also responsible for activation of the Arabidopsis thaliana innate immune system

International audienceSoft-rot diseases of plants attributed to Dickeya dadantii result from lysis of the plant cell wall caused by pectic enzymes released by the bacterial cell by a type II secretion system (T2SS). Arabidopsis thaliana can express several lines of defence against this bacterium. We employed bacterial mutants with defective envelope structures or secreted proteins to examine early plant defence reactions. We focused on the production of AtrbohD-dependent reactive oxygen species (ROS), callose deposition and cell death as indicators of these reactions. We observed a significant reduction in ROS and callose formation with a bacterial mutant in which genes encoding five pectate lyases (Pels) were disrupted. Treatment of plant leaves with bacterial culture filtrates containing Pels resulted in ROS and callose production, and both reactions were dependent on a functional AtrbohD gene. ROS and callose were produced in response to treatment with a cellular fraction of a T2SS-negative mutant grown in a Pels-inducing medium. Finally, ROS and callose were produced in leaves treated with purified Pels that had also been shown to induce the expression of jasmonic acid-dependent defence genes. Pel catalytic activity is required for the induction of ROS accumulation. In contrast, cell death observed in leaves infected with the wild-type strain appeared to be independent of a functional AtrbohD gene. It was also independent of the bacterial production of pectic enzymes and the type III secretion system (T3SS). In conclusion, the work presented here shows that D. dadantii is recognized by the A. thaliana innate immune system through the action of pectic enzymes secreted by bacteria at the site of infection. This recognition leads to AtrbohD-dependent ROS and callose accumulation, but not cell death