Abstract
Phytopathogens have a limited range of host plant species that they can successfully parasitise ie. that they are adapted for. Infection of plants by nonadapted pathogens often results in an active resistance response that is relatively poorly characterised because phenotypic variation in this response often does not exist within a plant species, or is too subtle for genetic dissection. In addition, complex polygenic inheritance often underlies these resistance phenotypes and mutagenesis often does not impact upon this resistance, presumably due to genetic or mechanistic redundancy. Here it is demonstrated that phenotypic differences in the resistance response of Brachypodium distachyon to the nonadapted wheat stripe rust pathogen Puccinia striiformis f. sp. tritici (Pst) are genetically tractable and simply inherited. Two dominant loci were identified on B. distachyon chromosome 4 that each reduce attempted Pst colonisation compared with sib and parent lines without these loci. One locus (Yrr1) is effective against diverse Australian Pst isolates and present in two B. distachyon mapping families as a conserved region that was reduced to 5 candidate genes by fine mapping. A second locus, Yrr2, shows Pst race-specificity and encodes a disease resistance gene family typically associated with host plant resistance. These data indicate that some components of resistance to nonadapted pathogens are genetically tractable in some instances and may mechanistically overlap with host plant resistance to avirulent adapted pathogens.
Highlights
A limited number of phytopathogen species are adapted to paracitise a given plant species
Pathogen infection of a plant that is not a host of the disease often results in an active plant defense response
Previous analysis of B. distachyon accessions BdTR10h and Tek-4 showed that macroscopically the former accession produced small brown lesions in response to challenge with Puccinia striiformis f. sp. tritici (Pst) pathotype 104 E137 A, whereas large, striped lesions were produced on Tek-4 plants [41] (Fig 1A and 1F)
Summary
A limited number of phytopathogen species are adapted to paracitise a given plant species. The numerous phyopathogens unable of colonising a plant species (nonadapted) are often suppressed by an active plant resistance response upon challenge [1, 2, 3, 4]. Plant resistance against nonadapted pathogens is considered durable as pathogen colonisation of new plant host species is rare, at least over short evolutionary time frames [5, 6]. Nonadapted pathogen infection can result in a variety of outcomes varying from complete plant immunity, to limited pathogen colonisation and reproduction [7]. Resistance to nonadapted pathogens can range from a basic physical or chemical incompatibility between a pathogen and potential plant host, to active recognition of pathogen challenge by the nonhost plant leading to a complex defense response [1, 8, 9, 10]. Current molecular models of active defense invoke similar mechanisms used to protect host plants against avirulent adapted pathogens, these being phytoalexin defences, callose deposition, reactive oxygen production and cell death in some instances [9, 10, 11]
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