Transcriptome analysis of a bacterially induced basal and hypersensitive response of Medicago truncatula.

Research using the well-studied model legume Medicago truncatula has largely focused on rhizobium symbiosis, while little information is currently available for this species on pathogen-induced transcriptome changes. We have performed a transcriptome analysis of this species with the objective of studying the basal (BR, no visible symptoms) and hypersensitive response (HR, plant cell death) in its leaves at 6 and at 24 h after infection by HR-negative (hrcC mutant) and HR-inducing Pseudomonas syringae pv. syringae strains, respectively.

Novel extracellular chitinases rapidly and specifically induced by general bacterial elicitors and suppressed by virulent bacteria as a marker of early basal resistance in tobacco.

Early basal resistance (EBR, formerly known as early induced resistance) is triggered by general bacterial elicitors. EBR has been suggested to inhibit or retard expression of the type III secretion system of pathogenic bacteria and may also prevent nonpathogenic bacteria from colonizing the plant tissue. The quickness of EBR here plays a crucial role, compensating for a low bactericidal efficacy.

Characterisation of basal resistance (BR) by expression patterns of newly isolated representative genes in tobacco.

Increasing evidence indicates that plants, like animals, use basal resistance (BR), a component of the innate immune system, to defend themselves against foreign organisms. Contrary to the hypersensitive reaction (HR)-type cell death, recognition in the case of BR is unspecific, as intruders are recognised based on their common molecular patterns. Induction of BR is not associated with visible symptoms, in contrast to the HR-type cell death.

Local early induced resistance of plants as the first line of defence against bacteria.

This paper is an overview of a non-specific local early induced resistance (EIR) mechanism, distinct from the incompatible-specific hypersensitive reaction (HR). We have shown that the local induced resistance (LIR) described earlier is not a single and uniform response to pathogen infection, because an early (EIR) and a late form can be distinguished. EIR operates from 3-6 h post-inoculation (hpi) until about 20 hpi, and is inhibited by a short heat-shock or the eukaryotic protein synthesis inhibitor, cycloheximide.