ABSTRACT
Background Plant disease resistance and susceptibility are governed by the combined genotypes of host and pathogen, and depend on a complex exchange of signals and responses occurring under given environmental conditions. During the long processes of host-pathogen co-evolution, plants have developed various elaborate mechanisms
to ward o pathogen attack [1]. A key dierence between resistant and susceptible plants is the timely recognition of the invading pathogen, and the rapid and eective activation of host defense mechanisms. e activation of defense responses in plants is initiated by host recognition of pathogen-encoded molecules called elicitors [2]. e interaction of pathogen elicitors with host receptors likely activates a signal transduction cascade that may involve protein phosphorylation, ion uxes, reactive oxygen species (ROS), and other signaling events [3,4]. Subsequent transcriptional and/or posttranslational activation of transcription factors eventually leads to the induction of plant defense related genes [5]. In addition to eliciting primary defense responses, pathogen signals may be amplied through the generation of secondary plant signal molecules such as salicylic acid [6]. Both primary pathogen elicitors and secondary endogenous signals may trigger a diverse array of plant defense related genes, encoding glutathione S-transferases (GST), peroxidases, cell wall proteins, proteinase inhibitors, hydrolytic enzymes, pathogenesisrelated (PR) proteins and phytoalexin biosynthetic enzymes [7].
