Genetic resistance to stripe rust infection of the wheat ear is controlled by genes controlling foliar resistance and flowering time

Abstract

Yellow rust (YR), or stripe rust, is a fungal infection of wheat (Triticum aestivum L.) caused by the pathogen Puccinia striiformis f. sp. tritici (Pst). While much research has focused on YR infection of wheat leaves, we are not aware of reports investigating the genetic control of YR resistance in other wheat structures, such as the ears. Here we use an eight-founder population to undertake genetic analysis of glume YR infection in wheat ears. Five quantitative trait loci (QTL) were identified, each explaining between 3.4% and 6.8% of the phenotypic variation. Of these, three (QYrg.niab-2D.1, QYrg.niab-4D.1 and QYrg.niab-5A.1) co-located with QTL for leaf YR resistance previously identified in the same population. Additional leaf YR resistance QTL previously identified in the population were not detected as controlling glume resistance, with the remaining two glume YR QTL linked to genetic loci controlling flowering time. The first, QYrg.niab-2D. 1, mapped to the major flowering time locus Photoperiod-D1 (Ppd-D1), with the early-flowering allele from the founder Soissons conferring reduced glume YR resistance. The second, QYrg.niab-4A.1, was identified in one trial only, and was located close to a flowering time QTL. This indicates earlier flowering results in increased glume YR susceptibility, likely due to exposure of tissues during environmental conditions more favourable for Pst infection. Collectively, our results provide first insights into the genetic control of YR resistance in glumes, ontrolled by subsets of QTL for leaf YR resistance and flowering time. This work provides specific genetic targets for the control of YR resistance in both the leaves and the glumes, and may be especially relevant in Pst-prone agricultural environments where earlier flowering is favoured.

The evolving battle between yellow rust and wheat: implications for global food security

“…Such APR race-specificity was initially reported by Johnson ( 1988 ) and has recently been observed in Europe following the spread of atypical Pst races (Sørensen et al 2014 ). For example, while the APR resistance allele conferred by the founder Claire at the QTL QYr.niab-2D.1 was effective in the UK during the 2015 and 2016 seasons (Bouvet et al 2021b ), it has since broken down (Simon Berry, personal communication). Another example is that of Yr49 , which was initially found to be non-race specific against all Australian Pst isolates, but when tested against Chinese races showed race-specificity (Ellis et al 2014 ).…”