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Wallwork, H.

Publications and source records attributed to Wallwork, H..

2 recordsLinked to original sources

Haplotype-based insights into the genetic architecture of net blotch resistance in barley

Net blotch, caused by Pyrenophora teres, is a major constraint to barley production worldwide and occurs as two epidemiologically distinct forms: net form net blotch (NFNB) and spot form net blotch (SFNB). Although numerous resistance loci have been reported in recent years, their genetic relationship remains poorly understood, and the effective deployment of resistance is constrained by the complex genetic architecture of net blotch resistance. In this study, we used a haplotype-based mapping approach to dissect the genetic basis of resistance to NFNB and SFNB in a diverse panel of 950 barley accessions from the Australian Grains Genebank (AGG). Disease responses were evaluated across 13 experiments, and a total of 40 quantitative trait loci (QTL) were identified, including 26 associated with NFNB, 29 with SFNB, and 15 common for both diseases. Most loci co-localized with previously reported QTL, while six putative novel haploblocks highlighted untapped genetic diversity within the AGG collection. Correlation analyses across phenotypic, genetic and haploblock levels revealed a partial but incomplete overlap in resistance mechanisms between NFNB and SFNB. Among the 4,497 haploblocks, approximately 60% of them showed positive local genetic correlations between the two diseases, suggesting shared genomic contributions to resistance. Haplotype composition analysis further identified a resistant haplotype group, mainly comprising accessions of Asian origin, that exhibited high levels of resistance to both forms of net blotch. Through in silico haplotype stacking, we demonstrated the cumulative genetic potential achievable by combining favourable haplotypes. When the breeding objective was to improve resistance to both NFNB and SFNB, dual-disease stacking strategies outperformed single-disease approaches, highlighting the value of prioritising haplotypes with positive pleiotropic effects. Overall, this study provides a comprehensive haplotype-level framework for understanding net blotch resistance and delivers practical insights for breeding barley cultivars with durable and broad-spectrum resistance to both NFNB and SFNB.

plant biology↗

Emergence of resistance to succinate dehydrogenase inhibitor fungicides in Pyrenophora teres f. teres and P. teres f. maculata in Australia

The net blotches are among the most economically significant diseases of barley worldwide. There are two forms of the disease: net-form net-blotch (NFNB, causal agent Pyrenophora teres f. sp. teres [Ptt]) and spot-form net blotch (SFNB, causal agent Pyrenophora teres f. sp. maculata [Ptm]). Alongside varietal choice and cultural practices, fungicides form an important part of the regime for net blotch control. The succinate dehydrogenase inhibitors (SDHIs) are a key class of fungicides used in net blotch management. However, resistance to this group of compounds has emerged in the net blotches in recent years. Here, we describe the first cases of resistance to SDHIs in Australian populations of net blotches. This study was prompted by reports of field failures of SDHI fungicides in controlling NFNB in South Australia and SFNB in Western Australia. Target site mutations in the Sdh complex genes, previously associated with reduced sensitivity in European net blotch populations, were found in Australian isolates, and two mutations which have not been previously observed in P. teres, are also described. The mutations found in Ptt included H134R and S135R in SdhC; and H134Y and D145G in SdhD; the SdhC-H134R mutation was the most frequently observed. In Ptm, the mutations found included H277L in SdhB; S73P, N75S, H134R and S135R in SdhC; and D145G in SdhD; the SdhC-N75S mutation was the most common. These mutations were correlated with reduced in vitro SDHI fungicide sensitivity by microtiter assay. The highest resistance factors to fluxapyroxad and bixafen, the most important SDHI fungicides for net blotch control in Australia, were associated with the SdhC-H134R and SdhC-S135R mutations in Ptt, and with the SdhB-H277L, SdhC-H134R, and SdhC-S135R mutations in Ptm. Modelling of the P. teres Sdh complex showed that the two novel mutations, H277L in SdhB and H134Y in SdhD, result in a highly altered binding mode and lower binding affinity of the SDHI compound compared to the wild-type.

microbiology↗