The genetic architecture of colonization resistance in Brachypodium distachyon to non-adapted stripe rust (Puccinia striiformis) isolates

Jan Bettgenhaeuser, Matthew Gardiner, Rebecca Spanner, Phon Green, Inmaculada Hernández-Pinzón, Amelia Hubbard, Michael Ayliffe, Matthew J. Moscou*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

Multilayered defense responses ensure that plants are hosts to only a few adapted pathogens in the environment. The host range of a plant pathogen depends on its ability to fully overcome plant defense barriers, with failure at any single step sufficient to prevent life cycle completion of the pathogen. Puccinia striiformis, the causal agent of stripe rust (=yellow rust), is an agronomically important obligate biotrophic fungal pathogen of wheat and barley. It is generally unable to complete its life cycle on the non-adapted wild grass species Brachypodium distachyon, but natural variation exists for the degree of hyphal colonization by Puccinia striiformis. Using three B. distachyon mapping populations, we identified genetic loci conferring colonization resistance to wheat-adapted and barley-adapted isolates of P. striiformis. We observed a genetic architecture composed of two major effect QTLs (Yrr1 and Yrr3) restricting the colonization of P. striiformis. Isolate specificity was observed for Yrr1, whereas Yrr3 was effective against all tested P. striiformis isolates. Plant immune receptors of the nucleotide binding, leucine-rich repeat (NB-LRR) encoding gene family are present at the Yrr3 locus, whereas genes of this family were not identified at the Yrr1 locus. While it has been proposed that resistance to adapted and non-adapted pathogens are inherently different, the observation of (1) a simple genetic architecture of colonization resistance, (2) isolate specificity of major and minor effect QTLs, and (3) NB-LRR encoding genes at the Yrr3 locus suggest that factors associated with resistance to adapted pathogens are also critical for non-adapted pathogens.

Original languageEnglish (US)
Article numbere1007637
JournalPLoS Genetics
Volume14
Issue number9
DOIs
StatePublished - Sep 2018

Bibliographical note

Funding Information:
Funding for the research described in this manuscript was contributed by the Gatsby Foundation (http://www.gatsby.org.uk/), the 2Blades Foundation (http://2blades.org/), Human Frontier Science Program (LT000218/2011-L; http://www.hfsp.org/), and the Biotechnology and Biological Sciences Research Council (BB/P012574/1 and BB/F017294/1). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. We thank John H. Doonan for access to the ABR6 x Bd21 population prior to publication, John P. Vogel for advance access to the Joint Genome Institute resequencing data, Pilar Catalán and Luis A. J. Mur for providing seed, Rosemary Bayles, Eric R. Ward, and Jonathan D. G. Jones for early discussions on the experimental design, Diane G. O. Saunders for discussions on the P. striiformis phylogeny, Brande B. H. Wulff and Paul Nicholson for helpful feedback and comments on the manuscript, Sue Banfield and the John Innes Centre Horticultural Service for assistance with plant growth, and Katie O’Neil for assistance with the Luc1 x Jer1 genetic map. KASP genotyping was performed at the John Innes Centre genotyping facility.

Publisher Copyright:
© 2018 Bettgenhaeuser et al. http://creativecommons.org/licenses/by/4.0/.

ASJC Scopus subject areas

  • Ecology, Evolution, Behavior and Systematics
  • Molecular Biology
  • Genetics
  • Genetics(clinical)
  • Cancer Research

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