Understanding the plant-pathogen interaction associated with Septoria nodorum blotch of wheat

This chapter discusses understanding the plant-pathogen interaction associated with septorium nodorum blotch of wheat. It begins by reviewing the necrotrophic effector-host sensitivity gene interactions in the wheat-P. nodorum system. It then reviews the genetic relationship between NE-sensitivity gene interactions and the importance of these interactions in the field. Additional QTL associated with susceptibility/resistance to P. nodorum is also discussed, followed by a section on the impact of genome sequencing in characterizing NE-sensitivity gene interactions.

Advances in genetic mapping of Septoria nodorum blotch resistance in wheat and applications in resistance breeding

Septoria nodorum blotch (SNB) caused by the necrotrophic fungus Parastagonospora nodorum is an important wheat disease in many high rainfall areas across the world. It reduces both yield and grain quality by causing symptoms on wheat leaves and glumes, and can cause yield losses up to 30% under warm and humid conditions. This book chapter gives an update on the recent progress in genetic mapping of SNB resistance in wheat, with focus on adult plant leaf blotch and glume blotch resistance with relevance to resistance breeding. This is followed by a case study on the investigation of the naturally occurring P. nodorum population in Norway and mapping of resistance loci in relevant wheat germplasm using MAGIC populations and GWAS panels as well as how this information can be used to improve resistance breeding and disease management. In the end, some future perspectives of SNB resistance breeding is provided.

Evaluation of Septoria Nodorum Blotch (SNB) Resistance in Glumes of Wheat (Triticum aestivum L.) and the Genetic Relationship With Foliar Disease Response

Septoria nodorum blotch (SNB) is a necrotrophic disease of wheat prominent in some parts of the world, including Western Australia (WA) causing significant losses in grain yield. The genetic mechanisms for resistance are complex involving multiple quantitative trait loci. In order to decipher comparable or independent regulation, this study identified the genetic control for glume compared to foliar resistance across four environments in WA against 37 different isolates. High proportion of the phenotypic variation across environments was contributed by genotype (84.0% for glume response and 82.7% for foliar response) with genotype-by-environment interactions accounting for a proportion of the variation for both glume and foliar response (14.7 and 16.2%, respectively). Despite high phenotypic correlation across environments, most of the eight and 14 QTL detected for glume and foliar resistance using genome wide association analysis (GWAS), respectively, were identified as environment-specific. QTL for glume and foliar resistance neither co-located nor were in LD in any particular environment indicating autonomous genetic mechanisms control SNB response in adult plants, regulated by independent biological mechanisms and influenced by significant genotype-by- environment interactions. Known Snn and Tsn loci and QTL were compared with 22 environment-specific QTL. None of the eight QTL for glume or the 14 for foliar response were co-located or in linkage disequilibrium with Snn and only one foliar QTL was in LD with Tsn loci on the physical map. Therefore, glume and foliar response to SNB in wheat is regulated by multiple environment-specific loci which function independently, with limited influence of known NE-Snn interactions for disease progression in Western Australian environments. Breeding for stable resistance would consequently rely on recurrent phenotypic selection to capture and retain favorable alleles for both glume and foliar resistance relevant to a particular environment.

Genes Associated with Foliar Resistance to Septoria Nodorum Blotch of Hexaploid Wheat (Triticum aestivum L.)

The genetic control of host response to the fungal necrotrophic disease Septoria nodorum blotch (SNB) in bread wheat is complex, involving many minor genes. Quantitative trait loci (QTL) controlling SNB response were previously identified on chromosomes 1BS and 5BL. The aim of this study, therefore, was to align and compare the genetic map representing QTL interval on 1BS and 5BS with the reference sequence of wheat and identify resistance genes (R-genes) associated with SNB response. Alignment of QTL intervals identified significant genome rearrangements on 1BS between parents of the DH population EGA Blanco, Millewa and the reference sequence of Chinese Spring with subtle rearrangements on 5BL. Nevertheless, annotation of genomic intervals in the reference sequence were able to identify and map 13 and 12 R-genes on 1BS and 5BL, respectively. R-genes discriminated co-located QTL on 1BS into two distinct but linked loci. NRC1a and TFIID mapped in one QTL on 1BS whereas RGA and Snn1 mapped in the linked locus and all were associated with SNB resistance but in one environment only. Similarly, Tsn1 and WK35 were mapped in one QTL on 5BL with NETWORKED 1A and RGA genes mapped in the linked QTL interval. This study provided new insights on possible biochemical, cellular and molecular mechanisms responding to SNB infection in different environments and also addressed limitations of using the reference sequence to identify the full complement of functional R-genes in modern varieties.

GWAS analysis reveals distinct pathogenicity profiles of Australian Parastagonospora nodorum isolates and identification of marker-trait-associations to septoria nodorum blotch

The fungus Parastagonospora nodorum is the causal agent of septoria nodorum leaf blotch (SNB) and glume blotch which are common in many wheat growing regions in the world. The disease is complex and could be explained by multiple interactions between necrotrophic effectors secreted by the pathogen and matching susceptibility genes in wheat. An Australian P. nodorum population was clustered into five groups with contrasting properties. This study was set to identify their pathogenicity profiles using a diverse wheat panel of 134 accessions which are insensitive to SnToxA and SnTox1 in both in vitro and in vivo conditions. SNB seedling resistance/susceptibility to five representative isolates from the five clusters, responses to crude culture-filtrates (CFs) of three isolates and sensitivity to SnTox3 semi-purified effector together with 11,455 SNP markers have been used for linkage disequilibrium (LD) and association analyses. While quantitative trait loci (QTL) on 1D, 2A, 2B, 4B, 5B, 6A, 6B, 7A, 7D chromosomes were consistently detected across isolates and conditions, distinct patterns and isolate specific QTL were also observed among these isolates. In this study, SnTox3–Snn3-B1 interaction for the first time in Australia and SnTox3–Snn3-D1 interaction for the first time in bread wheat were found active using wild-type isolates. These findings could be due to new SnTox3 haplotype/isoform and exotic CIMMYT/ICARDA and Vavilov germplasm used, respectively. This study could provide useful information for dissecting novel and different SNB disease components, helping to prioritise research targets and contributing valuable information on genetic loci/markers for marker-assisted selection in SNB resistance wheat breeding programme.

Evaluation of Septoria nodorum blotch (SNB) resistance in glumes of wheat (Triticum aestivum L.) in multiple field environments and the genetic relationship with foliar disease response

Septoria nodorum blotch (SNB) is a necrotrophic disease of wheat prominent in some parts of the world, including Western Australia (WA) causing significant losses in grain yield. The genetic mechanisms for resistance are complex involving multiple quantitative trait loci. In order to decipher comparable or independent regulation, this study identified the genetic control for glume compared to foliar resistance across four environments in WA against 37 different isolates. High proportion of the phenotypic variation across environments was contributed by genotype (84.0% for glume response and 82.7% for foliar response) with genotype-by-environment interactions accounting for a proportion of the variation for both glume and foliar response (14.7% and 16.2%, respectively). Despite high phenotypic correlation across environments, most of the eight and 14 QTL detected for glume and foliar resistance, respectively, were identified as environment-specific. QTL for glume and foliar resistance neither co-located nor were in LD in any particular environment indicating autonomous genetic mechanisms control SNB response in adult plants, regulated by independent biological mechanisms and influenced by significant genotype-by-isolate-by environment interactions. Known Snn and Tsn loci and QTL were compared with 22 environment-specific QTL. None of the eight QTL for glume or the 14 for foliar response were co-located or in linkage disequilibrium with Snn and only one foliar QTL was in LD with Tsn loci on the physical map. Therefore, known NE-Snn interactions are of limited relevance to glume and foliar SNB response in WA environments and other biological mechanisms are likely to prevail for host resistance and susceptibility.

Role of pathogen effectors SnTox in development of compatibility reaction in the pathosystem wheat – Stagonospora nodorum

It was shown that the interactions of SnToxA-Tsn1, SnTox1-Snn1 in the pathosystem wheat-Stagonospora nodorum play an important role in the development of Septoria nodorum blotch and are aimed at manipulating of host redox-status.

Septoria nodorum blotch of wheat: disease management and resistance breeding in the face of shifting disease dynamics and a changing environment

The fungus Parastagonospora nodorum is a narrow host range necrotrophic fungal pathogen that causes Septoria nodorum blotch (SNB) of cereals, most notably wheat. Although commonly observed on wheat seedlings, P. nodorum infection has the greatest effect on the adult crop. It results in leaf blotch, which limits photosynthesis and thus crop growth and yield. It can also affect the wheat ear, resulting in glume blotch which directly affects grain quality. Reports of P. nodorum fungicide resistance, the increasing use of reduced tillage agronomic practices and high evolutionary potential of the pathogen, combined with changes in climate and agricultural environments, mean that genetic resistance to SNB remains a high priority in many regions of wheat cultivation. In this review, we summarise current information on P. nodorum population structure and its implication for improved SNB management. We then review recent advances in the genetics of host resistance to P. nodorum and the necrotrophic effectors it secretes during infection, integrating the genomic positions of these genetic loci using the recently released wheat reference genome assembly. Finally, we discuss the genetic and genomic tools now available for SNB resistance breeding and consider future opportunities and challenges in crop health management using the wheat-P. nodorum interaction as a model.

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

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.