DspA/E-Triggered Non-Host Resistance against Depends on the Arabidopsis Gene.

DspA/E is a type three effector injected by the pathogenic bacterium inside plant cells. In non-host , DspA/E inhibits seed germination, root growth, de novo protein synthesis and triggers localized cell death. To better understand the mechanisms involved, we performed EMS mutagenesis on a transgenic line, 13-1-2, containing an inducible gene.

Plant nitrogen supply affects the Botrytis cinerea infection process and modulates known and novel virulence factors.

Plant nitrogen (N) fertilization is known to affect disease; however, the underlying mechanisms remain mostly unknown. We investigated the impact of N supply on the Arabidopsis thaliana-Botrytis cinerea interaction. A.

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

Soft-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.

Evolutionary tinkering of the expression of PDF1s suggests their joint effect on zinc tolerance and the response to pathogen attack.

Multigenic families of Plant Defensin type 1 (PDF1) have been described in several species, including the model plant Arabidopsis thaliana as well as zinc tolerant and hyperaccumulator A. halleri. In A.

Scavenging iron: a novel mechanism of plant immunity activation by microbial siderophores.

Siderophores are specific ferric iron chelators synthesized by virtually all microorganisms in response to iron deficiency. We have previously shown that they promote infection by the phytopathogenic enterobacteria Dickeya dadantii and Erwinia amylovora. Siderophores also have the ability to activate plant immunity.