Fine Mapping of the Barley Chromosome 6H Net Form Net Blotch Susceptibility Locus

Abstract

Net form net blotch, caused by the necrotrophic fungal pathogen Pyrenophora teres f. teres, is a destructive foliar disease of barley with the potential to cause significant yield loss in major production regions throughout the world. The complexity of the host–parasite genetic interactions in this pathosystem hinders the deployment of effective resistance in barley cultivars, warranting a deeper understanding of the interactions. Here, we report on the high-resolution mapping of the dominant susceptibility locus near the centromere of chromosome 6H in the barley cultivars Rika and Kombar, which are putatively targeted by necrotrophic effectors from P. teres f. teres isolates 6A and 15A, respectively. Utilization of progeny isolates derived from a cross of P. teres f. teres isolates 6A × 15A harboring single major virulence loci (VK1, VK2, and VR2) allowed for the Mendelization of single inverse gene-for-gene interactions in a high-resolution population consisting of 2976 Rika × Kombar recombinant gametes. Brachypodium distachyon synteny was exploited to develop and saturate the susceptibility region with markers, delimiting it to ∼0.24 cM and a partial physical map was constructed. This genetic and physical characterization further resolved the dominant susceptibility locus, designated Spt1 (susceptibility to P. teres f. teres). The high-resolution mapping and cosegregation of the Spt1.R and Spt1.K gene/s indicates tightly linked genes in repulsion or alleles possibly targeted by different necrotrophic effectors. Newly developed barley genomic resources greatly enhance the efficiency of positional cloning efforts in barley, as demonstrated by the Spt1 fine mapping and physical contig identification reported here.

Resistance to Pyrenophora teres f. teres and P. teres f. maculata in Canadian Barley Genotypes

“…It was reported that sensitivity to a proteinaceous necrotrophic effector, produced by Ptt and mapped to barley chromosome 6H, was responsible for 31% of the variation observed in disease (Liu et al, 2015). These findings collectively emphasize the complexity of the host-parasite genetic interactions in this pathosystem and suggest that barley breeding programs should also consider eliminating dominant susceptibility genes or genes inducing necrotrophic effector-triggered susceptibility to develop Ptt-resistant cultivars (Liu et al, 2015;Richards et al, 2016). It is possible that differential production of this necrotrophic effector contributes to the virulence of different isolates of Ptt.…”

“…The seven Ptt and Ptm isolates examined represented six and five different pathotype groups, respectively, including the predominant pathotype groups C4 and E9 for Ptt and V1 and T1 for Ptm (Table 1). Moreover, the pathogen and host genotype interaction in this pathosystem is very complex and still not well understood (Liu et al, 2015;Richards et al, 2016). No clear pattern was observed in a recent study with respect to the geographic distribution of Ptt and Ptm pathotypes across the Canadian prairies (Akhavan et al, 2016a).…”

“…Pathotype distribution in each region is difficult to assess, particularly on a regular basis. Moreover, the pathogen and host genotype interaction in this pathosystem is very complex and still not well understood (Liu et al, 2015;Richards et al, 2016). Therefore, we used the overall mean disease reactions for each host genotype and isolate to compare the relative virulence and resistance of isolates and host genotypes, respectively, as well as specific interactions.…”

“…The authors concluded that there was a specific, rather than a generalized, NFNB resistance mechanism. Very recently, Richards et al (2016) also mapped a dominant susceptibility locus close to the centromere of chromosome 6H, which presumably can be targeted by Ptt necrotrophic effectors. As a result of this finding, it was proposed that the barley-Ptt pathosystem follows, at least partially, a necrotrophic effector-triggered susceptibility model (Liu et al, 2015).…”

“…It is possible that differential production of this necrotrophic effector contributes to the virulence of different isolates of Ptt. Very recently, Richards et al (2016) also mapped a dominant susceptibility locus close to the centromere of chromosome 6H, which presumably can be targeted by Ptt necrotrophic effectors. These findings collectively emphasize the complexity of the host-parasite genetic interactions in this pathosystem and suggest that barley breeding programs should also consider eliminating dominant susceptibility genes or genes inducing necrotrophic effector-triggered susceptibility to develop Ptt-resistant cultivars (Liu et al, 2015;Richards et al, 2016).…”