Priming Arabidopsis for defense : Molecular and ecological aspects

Abstract

Plants are capable to enhance basal defense strategies against harmful organisms upon the perception of certain stimuli. This enhanced resistance is not necessarily accompanied by direct activation of defenses, but often depends on a sensitization of the plant tissue to express defenses faster and/or stronger when the plant is under attack. In analogy with a similar phenomenon in animals, this is commonly called priming. This thesis describes that priming induced in the model plant Arabidopsis thaliana by exogenous application of the non-protein amino acid ?-aminobutyric acid (BABA) or root colonization by the non-pathogenic rhizobacterium Pseudomonas fluorescens WCS417r is accompanied by direct transcriptional activation of distinct sets of transciptionfactor (TF) genes. It is believed that these TFs will further remain inactive until subsequent pathogen attack, when they will enhance the expression of salicylic acid (SA)- and jasmonic acid (JA)-dependent defenses, respectively. BABA induced the expression of 22 out of the 72 known WRKY TF genes, mostly in a NPR1-dependent manner. This fits the SA-dependency of resistance induced by BABA (BABA-IR), since WRKYs are key transcriptional regulators of SA-dependent defenses. Promoter analysis identified an overrepresentation of a certain motif in the promoters of these BABA-inducible WRKY genes. This motif, TAG[TA]CT, may represent an important cis-acting element in BABA-induced priming of SA-dependent defenses. However, BABA also primes SA-independent cell wall defense, resulting in an enhanced deposition of callose containing papillae in response to fungal or oomycetal penetration. This priming for cell wall defense by BABA is dependent on intact absicic acid (ABA) and phosphoinositide signaling. In order to identify novel regulators involved in BABA-induced priming of callose depositions, an ethylmethance sulfonate (EMS)-mutagenesis screen was set up to identify mutants impaired in BABA-induced immunity (ibi). This resulted in the identification of ibi1, whose mutation maps to the lower arm of chromosome 4. IBI1 acts likely upstream of or parallel to ABA. Preliminary results points towards a possible role for IBI1 in the regulation of the redox state of the cell. Further characterization of ibi1 will lead to new insights in BABA-induced priming of cell wall defense. A cost-benefit analysis of priming indicated that priming is a cost-efficient method for plants to protect themselves in regions with high disease incidence, since priming induces only marginal trade-offs on growth and seed set under enemy free conditions. The existence of natural Arabidopsis accessions that have genetically acquired a primed capacity to express SA- and/or JA-dependent defenses fits the hypothesis that priming seems a beneficial strategy for plants in hostile environments. The question remains whether plants grown in nature have already acquired a primed defensive capacity. A preliminary field experiment indeed showed that wild-type plants may have acquired a primed defensive capacity under the specific environmental conditions of that field experiment, although more field-experiments should be conducted to study the extent and the conditions of priming in crop plants. A better understanding of the priming phenomenon may ultimately lead to the use of priming as a durable protection strategy in agriculture.