Discovery of genes affecting resistance of barley to adapted and non-adapted powdery mildew fungi.

Dimitar Douchkov,Daniela Nowara,Stefanie Lück,Jeyaraman Rajaraman,Patrick Schweizer,Benjamin Kilian,Nils Stein,Annika Johrde,Rajiv Sharma,Axel Himmelbach

doi:10.1186/s13059-014-0518-8

Abstract

BackgroundNon-host resistance, NHR, to non-adapted pathogens and quantitative host resistance, QR, confer durable protection to plants and are important for securing yield in a longer perspective. However, a more targeted exploitation of the trait usually possessing a complex mode of inheritance by many quantitative trait loci, QTLs, will require a better understanding of the most important genes and alleles.ResultsHere we present results from a transient-induced gene silencing, TIGS, approach of candidate genes for NHR and QR in barley against the powdery mildew fungus Blumeria graminis. Genes were selected based on transcript regulation, multigene-family membership or genetic map position. Out of 1,144 tested RNAi-target genes, 96 significantly affected resistance to the non-adapted wheat- or the compatible barley powdery mildew fungus, with an overlap of four genes. TIGS results for QR were combined with transcript regulation data, allele-trait associations, QTL co-localization and copy number variation resulting in a meta-dataset of 51 strong candidate genes with convergent evidence for a role in QR.ConclusionsThis study represents an initial, functional inventory of approximately 3% of the barley transcriptome for a role in NHR or QR against the powdery mildew pathogen. The discovered candidate genes support the idea that QR in this Triticeae host is primarily based on pathogen-associated molecular pattern-triggered immunity, which is compromised by effector molecules produced by the compatible pathogen. The overlap of four genes with significant TIGS effects both in the NHR and QR screens also indicates shared components for both forms of durable pathogen resistance.Electronic supplementary materialThe online version of this article (doi:10.1186/s13059-014-0518-8) contains supplementary material, which is available to authorized users.

Highlights

Non-host resistance, non-host resistance (NHR), to non-adapted pathogens and quantitative host resistance, quantitative resistance (QR), confer durable protection to plants and are important for securing yield in a longer perspective
Selection of gene groups In total 1,274 transient-induced gene silencing (TIGS) constructs were bombarded into barley epidermal cells, which corresponded to 1,144 candidate target genes due to a certain number of redundant constructs targeting the same genes
The sets of TIGS constructs used in both screens overlapped partially and targeted primarily transcripts found to be upregulated during host or non-host interactions of barley epidermis with Blumeria graminis f.sp. hordei (Bgh) or B. graminis f.sp. tritici (Bgt). (Table 1)

Summary

Introduction

Non-host resistance, NHR, to non-adapted pathogens and quantitative host resistance, QR, confer durable protection to plants and are important for securing yield in a longer perspective. Plant-pathogen co-evolution has shaped a multifaceted innate immunity system triggered by the recognition of non-self-molecules via pathogen recognition receptors (PRRs) belonging to the family of receptor-like kinases (RLKs) [1] These non-self-molecules known as pathogenassociated molecular patterns (PAMPs) or, more generally, microbe-associated molecular patterns (MAMPs) include conserved domains of proteins such as bacterial flagellin (flg22) or chitin fragments from fungal cell walls [2]. Durable and broad-range non-host resistance (NHR) to virtually all races of non-adapted pathogens appears to be an important manifestation of PTI in many cases [4,5] there is experimental evidence that NHR can - at least in grass species - be mediated by as little as one major R gene recognizing an indispensable Avr effector [6]. QR could be mediated by partially functional (defeated) major R-genes weakly recognizing ubiquitous Avr effectors such as ECP1 or ECP2 [12], but molecular evidence for this type of interactions is scarce [13,14]

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