Induced resistance protects plants against a wide spectrum of diseases; however, it can also entail costs due to the allocation of resources or toxicity of defensive products. The cellular defense responses involved in induced resistance are either activated directly or primed for augmented expression upon pathogen attack. Priming for defense may combine the advantages of enhanced disease protection and low costs. In this study, we have compared the costs and benefits of priming to those of induced direct defense in Arabidopsis. In the absence of pathogen infection, chemical priming by low doses of ␤-aminobutyric acid caused minor reductions in relative growth rate and had no effect on seed production, whereas induction of direct defense by high doses of ␤-aminobutyric acid or benzothiadiazole strongly affected both fitness parameters. These costs were defense-related, because the salicylic acid-insensitive defense mutant npr1-1 remained unaffected by these treatments. Furthermore, the constitutive priming mutant edr1-1 displayed only slightly lower levels of fitness than wild-type plants and performed considerably better than the constitutively activated defense mutant cpr1-1. Hence, priming involves less fitness costs than induced direct defense. Upon infection by Pseudomonas syringae or Hyaloperonospora parasitica, priming conferred levels of disease protection that almost equaled the protection in benzothiadiazole-treated wild-type plants and cpr1 plants. Under these conditions, primed plants displayed significantly higher levels of fitness than noninduced plants and plants expressing chemically or cpr1-induced direct defense. Collectively, our results indicate that the benefits of priming-mediated resistance outweigh the costs in environments in which disease occurs.induced resistance ͉ innate immunity ͉ plant defense

Specific chemicals can prime the plant immune system for augmented defence. β-aminobutyric acid (BABA) is a priming agent that provides broad-spectrum disease protection. However, BABA also suppresses plant growth when applied in high doses, which has hampered its application as a crop defence activator. Here we describe a mutant of Arabidopsis thaliana that is impaired in BABA-induced disease immunity (ibi1) but hypersensitive to BABA-induced growth repression. IBI encodes an aspartyl-tRNA synthetase. Enantiomer-specific binding of R-BABA to IBI1 primed the protein for non-canonical defence signalling in the cytoplasm after pathogen attack. This priming was associated with aspartic acid accumulation and tRNA-induced phosphorylation of translation initiation factor eIF2α. However, mutation of eIF2α-phosphorylating GCN2 kinase did not affect BABA-induced immunity, but relieved BABA-induced growth repression. Hence, BABA-activated IBI1 controls plant immunity and growth via separate pathways. Our results open new opportunities to separate broad-spectrum disease resistance from the associated costs on plant growth.

Summary• Pseudomonas fluorescens WCS417r bacteria and β-aminobutyric acid can induce disease resistance in Arabidopsis, which is based on priming of defence.• In this study, we examined the differences and similarities of WCS417r-and β-aminobutyric acid-induced priming.• Both WCS417r and β-aminobutyric acid prime for enhanced deposition of callose-rich papillae after infection by the oomycete Hyaloperonospora arabidopsis. This priming is regulated by convergent pathways, which depend on phosphoinositideand ABA-dependent signalling components. Conversely, induced resistance by WCS417r and β-aminobutyric acid against the bacterial pathogen Pseudomonas syringae are controlled by distinct NPR1-dependent signalling pathways. As WCS417r and β-aminobutyric acid prime jasmonate-and salicylate-inducible genes, respectively, we subsequently investigated the role of transcription factors. A quantitative PCR-based genome-wide screen for putative WCS417r-and β-aminobutyric acid-responsive transcription factor genes revealed distinct sets of priming-responsive genes. Transcriptional analysis of a selection of these genes showed that they can serve as specific markers for priming. Promoter analysis of WRKY genes identified a putative cis-element that is strongly over-represented in promoters of 21 NPR1-dependent, β-aminobutyric acid-inducible WRKY genes.• Our study shows that priming of defence is regulated by different pathways, depending on the inducing agent and the challenging pathogen. Furthermore, we demonstrated that priming is associated with the enhanced expression of transcription factors.

Basal resistance involves a multitude of pathogen-and herbivore-inducible defence mechanisms, ranging from localized callose deposition to systemic defence gene induction by salicylic acid (SA) and jasmonic acid (JA). In this study, we have explored and dissected genetic variation in the responsiveness of basal defence mechanisms within a selection of Arabidopsis accessions. Responsiveness of JA-induced PDF1.2 gene expression was associated with enhanced basal resistance against the necrotrophic fungus Plectosphaerella cucumerina and the herbivore Spodoptera littoralis. Conversely, accessions showing augmented PR-1 induction upon SA treatment were more resistant to the hemi-biotrophic pathogen Pseudomonas syringae, and constitutively expressed defence-related transcription factor (TF) genes. Unexpectedly, accessions with primed responsiveness to SA deposited comparatively little callose after treatment with microbe-associated molecular patterns. A quantitative trait locus (QTL) analysis identified two loci regulating flagellin-induced callose and one locus regulating SA-induced PR-1 expression. The latter QTL was found to contribute to basal resistance against P. syringae. None of the defence regulatory QTLs influenced plant growth, suggesting that the constitutive defence priming conferred by these loci is not associated with major costs on plant growth. Our study demonstrates that natural variation in basal resistance can be exploited to identify genetic loci that prime the plant's basal defence arsenal.