Molecular aspects of plant systemic immunity

Plants have to cope with changing environmental conditions throughout their lifetime. To successfully grow and develop, they must adequately respond to a variety of biotic and abiotic factors. For instance, plants are equipped with an intricate defence network with which they counteract attempted invasion by bacterial, fungal, or viral plant pathogens. Our research group is interested in the molecular responses that plants activate after having recognized such microbial invaders. These responses are not confined to the initial site of microbial attack but can extend to other plant parts. For instance, the entire plant shoot system is able to develop an enhanced state of broad-spectrum disease resistance after a single leaf has encountered an infection with a biotrophic or hemibiotrophic plant pathogen. This phenomenon, termed systemic acquired resistance (SAR), has been recognized in many different plants species. The model plant Arabidopsis thaliana exhibits a robust SAR response when cultivated under adequate, low-stress conditions and infected with an inducing microbe such as the hemibiotrophic bacterial pathogen Pseudomonas syringae (Fig. 1).

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The physiological and molecular mechanisms underlying SAR are only fragmentarily understood. A hallmark of the SAR response is its dependence on the plants’ ability to synthesize the defense hormone salicylic acid (SA) which activates expression of SAR-related genes. To further understand the SAR phenomenon at the molecular level, it is advantageous to formally divide the process into three consecutive stages (Fig.2):

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The initiation of SAR at the infection site

One of the first events accounting for SAR induction in Arabidopsis upon P. syringae infection is the perception of conserved bacterial elicitors (also called pathogen-associated molecular patterns, PAMPs) such as flagellin or lipopolysaccharides (Mishina and Zeier, 2007). In addition, signaling events associated with the hypersensitive response following recognition of specific avirulence signals is thought to contribute to SAR induction. During SAR initiation, one or more transmissible, metabolic signals are supposed to be generated. One aim of our research is therefore to elucidate the metabolic and biochemical changes that occur in pathogen-infected leaves and to assess their relevance during the establishment of plant systemic immunity (e.g. Griebel and Zeier, 2010; Attaran et al., 2008).

The movement of the mobile SAR signal(s) through the vascular system to distant, non-infected (systemic) tissue

Although SA is a central SAR metabolite produced in infected and in systemic leaves, it is not a mobile long-distance signal. Other putative signals have been suggested during the last decade, but the chemical basis of SAR long-distance signaling is still enigmatic. Our recent findings have disproven previous reports that the plant hormone jasmonic acid and/or the methylated form of SA, methyl salicylate, would act as mobile SAR signals in Arabidopsis (Attaran et al., 2009). Through comparative metabolite analyses of exudates collected from pathogen-treated and control leaves, we aim to get further insight into the nature of SAR long-distance signaling.

The perception and amplification of these signal(s) in distant leaves to trigger systemic defense responses and ensure an enhanced state of resistance

A recent microarray analyses has revealed that SAR is associated with a massive transcriptional reprogramming at the systemic level. An essential component that mediates these changes is FLAVIN-DEPENDENT MONOOXYGENASE1 (FMO1) (Mishina and Zeier, 2006). Although the biochemical function of FMO1 is still unclear, we assume that the monooxygenase contributes to a signal amplification mechanism in systemic plant parts that drives de novo SA biosynthesis, expression of SAR genes and mobilization of further defense responses during SAR.

Head of Institute

Prof. Dr. Jürgen Zeier

Molekulare Ökophysiologie der Pflanzen
Heinrich-Heine-Universität
Düsseldorf
Universitätsstraße 1
Building: 26.13
Floor/Room: 00.74
40225 Düsseldorf
Phone +49 211 81-14733
Responsible for the content: E-MailProf. Dr. Jürgen Zeier