Identification and cross-validation of genetic loci conferring resistance to Septoria nodorum blotch using a German multi-founder winter wheat population

Abstract

Key message We identified allelic variation at two major loci, QSnb.nmbu-2A.1 and QSnb.nmbu-5A.1, showing consistent and additive effects on SNB field resistance. Validation of QSnb.nmbu-2A.1 across genetic backgrounds further highlights its usefulness for marker-assisted selection. Abstract Septoria nodorum blotch (SNB) is a disease of wheat (Triticum aestivum and T. durum) caused by the necrotrophic fungal pathogen Parastagonospora nodorum. SNB resistance is a typical quantitative trait, controlled by multiple quantitative trait loci (QTL) of minor effect. To achieve increased plant resistance, selection for resistance alleles and/or selection against susceptibility alleles must be undertaken. Here, we performed genetic analysis of SNB resistance using an eight-founder German Multiparent Advanced Generation Inter-Cross (MAGIC) population, termed BMWpop. Field trials and greenhouse testing were conducted over three seasons in Norway, with genetic analysis identifying ten SNB resistance QTL. Of these, two QTL were identified over two seasons: QSnb.nmbu-2A.1 on chromosome 2A and QSnb.nmbu-5A.1 on chromosome 5A. The chromosome 2A BMWpop QTL co-located with a robust SNB resistance QTL recently identified in an independent eight-founder MAGIC population constructed using varieties released in the United Kingdom (UK). The validation of this SNB resistance QTL in two independent multi-founder mapping populations, regardless of the differences in genetic background and agricultural environment, highlights the value of this locus in SNB resistance breeding. The second robust QTL identified in the BMWpop, QSnb.nmbu-5A.1, was not identified in the UK MAGIC population. Combining resistance alleles at both loci resulted in additive effects on SNB resistance. Therefore, using marker assisted selection to combine resistance alleles is a promising strategy for improving SNB resistance in wheat breeding. Indeed, the multi-locus haplotypes determined in this study provide markers for efficient tracking of these beneficial alleles in future wheat genetics and breeding activities.

Genome-wide association analysis permits characterization of Stagonospora nodorum blotch (SNB) resistance in hard winter wheat

“…We identified one QTL ( QSnb.sdsu-2D ) on the short arm of chromosome 2D, which physically maps to 9 Mb on the wheat reference genome. Two recent studies 53 , 54 have also reported SNB resistance QTLs in the same region (~ 14–15 Mb) at the adult plant stage. This region also harbors the SnTox2 sensitivity gene Snn2 (6–12 Mb) 53 ; thus, QSnb.sdsu-2D identified in this study co-locates with this sensitivity gene.…”

“…The current study also validated another genomic region on chromosome 2AL at ~ 780 Mb. Several studies have identified loci for seedling and adult plant resistance in the same region 20 , 47 , 53 , 54 . In a very recent report, Lin et al 53 identified an adult plant resistance QTL in the same region positioned between 755 and 780 Mb, overlapping with the QSnb.sdsu.2A .…”

Variability in an effector gene promoter of a necrotrophic fungal pathogen dictates epistasis and effector-triggered susceptibility in wheat

“…The physical interval for Qsnb.cur–2AS1 is notably large (22). Nevertheless, several recent studies suggest the locus contains a gene conferring sensitivity to an undiscovered NE, that functions as an important determinant of both seedling, adult leaf and glume SNB resistance since these QTL overlap with Qsnb.cur–2AS1 (20, 22, 26, 54). In addition, a minor seedling resistance QTL on chromosome 2A was detected in a recombinant inbred population derived from Swiss winter wheat varieties Arina and Forno (20).…”

“…For instance, Tan et al (8) demonstrated that the deletion of ToxA, Tox1 and Tox3 in P. nodorum SN15 did not significantly alter virulence on a diverse collection of modern wheat varieties (8,9). A further complication in breeding for SNB resistance is that some NE-host gene interactions were not consistently detected in field trials using mapping populations with known susceptibility genes (25,26). It is intuitive to hypothesise that NE epistasis plays a significant role in shaping the variations observed in host resistance to SNB (Table 1) (27).…”

Variability in an effector gene promoter of a necrotrophic fungal pathogen dictates epistasis and effector-triggered susceptibility in wheat

“…nodorum SN15 did not significantly alter virulence on a diverse collection of modern wheat varieties [ 8 , 9 ]. A further complication in breeding for SNB resistance is that some NE-host gene interactions were not consistently detected in field trials using mapping populations with known susceptibility genes [ 25 , 26 ]. It is intuitive to hypothesise that NE epistasis plays a significant role in shaping the variations observed in host resistance to SNB ( Table 1 ) [ 27 ].…”