Longer epidermal cells underlie a quantitative source of variation in wheat flag leaf size.

The wheat flag leaf is the main contributor of photosynthetic assimilates to developing grains. Understanding how canopy architecture strategies affect source strength and yield will aid improved crop design. We used an eight-founder population to investigate the genetic architecture of flag leaf area, length, width and angle in European wheat. For the strongest genetic locus identified, we subsequently created a near-isogenic line (NIL) pair for more detailed investigation across seven test environments. Genetic control of traits investigated was highly polygenic, with colocalisation of replicated quantitative trait loci (QTL) for one or more traits identifying 24 loci. For QTL QFll.niab-5A.1 (FLL5A), development of a NIL pair found the FLL5A+ allele commonly conferred a c. 7% increase in flag and second leaf length and a more erect leaf angle, resulting in higher flag and/or second leaf area. Increased FLL5A-mediated flag leaf length was associated with: (1) longer pavement cells and (2) larger stomata at lower density, with a trend for decreased maximum stomatal conductance (Gsmax ) per unit leaf area. For FLL5A, cell size rather than number predominantly determined leaf length. The observed trade-offs between leaf size and stomatal morphology highlight the need for future studies to consider these traits at the whole-leaf level.

Identification of eight QTL controlling multiple yield components in a German multi-parental wheat population, including Rht24, WAPO-A1, WAPO-B1 and genetic loci on chromosomes 5A and 6A.

KEY MESSAGE: Quantitative trait locus (QTL) mapping of 15 yield component traits in a German multi-founder population identified eight QTL each controlling ≥2 phenotypes, including the genetic loci Rht24, WAPO-A1 and WAPO-B1. Grain yield in wheat (Triticum aestivum L.) is a polygenic trait representing the culmination of many developmental processes and their interactions with the environment. Toward maintaining genetic gains in yield potential, 'reductionist approaches' are commonly undertaken by which the genetic control of yield components, that collectively determine yield, are established. Here we use an eight-founder German multi-parental wheat population to investigate the genetic control and phenotypic trade-offs between 15 yield components. Increased grains per ear was significantly positively correlated with the number of fertile spikelets per ear and negatively correlated with the number of infertile spikelets. However, as increased grain number and fertile spikelet number per ear were significantly negatively correlated with thousand grain weight, sink strength limitations were evident. Genetic mapping identified 34 replicated quantitative trait loci (QTL) at two or more test environments, of which 24 resolved into eight loci each controlling two or more traits-termed here 'multi-trait QTL' (MT-QTL). These included MT-QTL associated with previously cloned genes controlling semi-dwarf plant stature, and with the genetic locus Reduced height 24 (Rht24) that further modulates plant height. Additionally, MT-QTL controlling spikelet number traits were located to chromosome 7A encompassing the gene WHEAT ORTHOLOG OF APO1 (WAPO-A1), and to its homoeologous location on chromosome 7B containing WAPO-B1. The genetic loci identified in this study, particularly those that potentially control multiple yield components, provide future opportunities for the targeted investigation of their underlying genes, gene networks and phenotypic trade-offs, in order to underpin further genetic gains in yield.

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 (Triticum aestivum). 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 summarize 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 by 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 by using the wheat-P. nodorum interaction as a model.

Genetic mapping using a wheat multi-founder population reveals a locus on chromosome 2A controlling resistance to both leaf and glume blotch caused by the necrotrophic fungal pathogen Parastagonospora nodorum.

KEY MESSAGE: A locus on wheat chromosome 2A was found to control field resistance to both leaf and glume blotch caused by the necrotrophic fungal pathogen Parastagonospora nodorum. The necrotrophic fungal pathogen Parastagonospora nodorum is the causal agent of Septoria nodorum leaf blotch and glume blotch, which are common wheat (Triticum aestivum L.) diseases in humid and temperate areas. Susceptibility to Septoria nodorum leaf blotch can partly be explained by sensitivity to corresponding P. nodorum necrotrophic effectors (NEs). Susceptibility to glume blotch is also quantitative; however, the underlying genetics have not been studied in detail. Here, we genetically map resistance/susceptibility loci to leaf and glume blotch using an eight-founder wheat multiparent advanced generation intercross population. The population was assessed in six field trials across two sites and 4 years. Seedling infiltration and inoculation assays using three P. nodorum isolates were also carried out, in order to compare quantitative trait loci (QTL) identified under controlled conditions with those identified in the field. Three significant field resistance QTL were identified on chromosomes 2A and 6A, while four significant seedling resistance QTL were detected on chromosomes 2D, 5B and 7D. Among these, QSnb.niab-2A.3 for field resistance to both leaf blotch and glume blotch was detected in Norway and the UK. Colocation with a QTL for seedling reactions against culture filtrate from a Norwegian P. nodorum isolate indicated the QTL could be caused by a novel NE sensitivity. The consistency of this QTL for leaf blotch at the seedling and adult plant stages and culture filtrate infiltration was confirmed by haplotype analysis. However, opposite effects for the leaf blotch and glume blotch reactions suggest that different genetic mechanisms may be involved.

Genetic analysis of wheat sensitivity to the ToxB fungal effector from Pyrenophora tritici-repentis, the causal agent of tan spot.

KEY MESSAGE: Genetic mapping of sensitivity to the Pyrenophora tritici-repentis effector ToxB allowed development of a diagnostic genetic marker, and investigation of wheat pedigrees allowed transmission of sensitive alleles to be tracked. Tan spot, caused by the necrotrophic fungal pathogen Pyrenophora tritici-repentis, is a major disease of wheat (Triticum aestivum). Secretion of the P. tritici-repentis effector ToxB is thought to play a part in mediating infection, causing chlorosis of plant tissue. Here, genetic analysis using an association mapping panel (n = 480) and a multiparent advanced generation intercross (MAGIC) population (n founders = 8, n progeny = 643) genotyped with a 90,000 feature single nucleotide polymorphism (SNP) array found ToxB sensitivity to be highly heritable (h2 ≥ 0.9), controlled predominantly by the Tsc2 locus on chromosome 2B. Genetic mapping of Tsc2 delineated a 1921-kb interval containing 104 genes in the reference genome of ToxB-insensitive variety 'Chinese Spring'. This allowed development of a co-dominant genetic marker for Tsc2 allelic state, diagnostic for ToxB sensitivity in the association mapping panel. Phenotypic and genotypic analysis in a panel of wheat varieties post-dated the association mapping panel further supported the diagnostic nature of the marker. Combining ToxB phenotype and genotypic data with wheat pedigree datasets allowed historic sources of ToxB sensitivity to be tracked, finding the variety 'Maris Dove' to likely be the historic source of sensitive Tsc2 alleles in the wheat germplasm surveyed. Exploration of the Tsc2 region gene space in the ToxB-sensitive line 'Synthetic W7984' identified candidate genes for future investigation. Additionally, a minor ToxB sensitivity QTL was identified on chromosome 2A. The resources presented here will be of immediate use for marker-assisted selection for ToxB insensitivity and the development of germplasm with additional genetic recombination within the Tsc2 region.

Genetic Dissection of Resistance to the Three Fungal Plant Pathogens Blumeria graminis, Zymoseptoria tritici, and Pyrenophora tritici-repentis Using a Multiparental Winter Wheat Population.

Bread wheat (Triticum aestivum L.) is one of the world's most important crop species. The development of new varieties resistant to multiple pathogens is an ongoing task in wheat breeding, especially in times of increasing demand for sustainable agricultural practices. Despite this, little is known about the relations between various fungal disease resistances at the genetic level, and the possible consequences for wheat breeding strategies. As a first step to fill this gap, we analyzed the genetic relations of resistance to the three fungal diseases - powdery mildew (PM), septoria tritici blotch (STB), and tan spot (TS) - using a winter wheat multiparent advanced generation intercross population. Six, seven, and nine QTL for resistance to PM, STB, and TS, respectively, were genetically mapped. Additionally, 15 QTL were identified for the three agro-morphological traits plant height, ear emergence time, and leaf angle distribution. Our results suggest that resistance to STB and TS on chromosome 2B is conferred by the same genetic region. Furthermore, we identified two genetic regions on chromosome 1AS and 7AL, which are associated with all three diseases, but not always in a synchronal manner. Based on our results, we conclude that parallel marker-assisted breeding for resistance to the fungal diseases PM, STB, and TS appears feasible. Knowledge of the genetic co-localization of alleles with contrasting effects for different diseases, such as on chromosome 7AL, allows the trade-offs of selection of these regions to be better understood, and ultimately determined at the genic level.