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Wheat production is threatened by multiple fungal pathogens, such as the wheat powdery mildew fungus (Blumeria graminis f. sp. tritici, Bgt). Wheat resistance breeding frequently relies on the use of resistance (R) genes that encode diverse immune receptors which detect specific avirulence (AVR) effectors and subsequently induce an immune response. While R gene cloning has accelerated recently, AVR identification in many pathogens including Bgt lags behind, preventing pathogen-informed deployment of resistance sources. Here we describe a new "avirulence depletion (AD) assay" for rapid identification of AVR genes in Bgt. This assay relies on the selection of a segregating, haploid F1 progeny population on a resistant host, followed by bulk sequencing, thereby allowing rapid avirulence candidate gene identification with high mapping resolution. In a proof-of-concept experiment we mapped the AVR component of the wheat immune receptor Pm3a to a 25 kb genomic interval in Bgt harboring a single effector, the previously described AvrPm3a2/f2. Subsequently, we applied the AD assay to map the unknown AVR effector recognized by the Pm60 immune receptor. We show that AvrPm60 is encoded by three tandemly arrayed, nearly identical effector genes that trigger an immune response upon co-expression with Pm60 and its alleles Pm60a and Pm60b. We furthermore provide evidence that Pm60 outperforms Pm60a and Pm60b through more efficient recognition of AvrPm60 effectors, suggesting it should be prioritized for wheat breeding. Finally, we show that virulence towards Pm60 is caused by simultaneous deletion of all AvrPm60 gene paralogs and that isolates lacking AvrPm60 are especially prevalent in the US thereby limiting the potential of Pm60 in this region. The AD assay is a powerful new tool for rapid and inexpensive AVR identification in Bgt with the potential to contribute to pathogen-informed breeding decisions for the use of novel R genes and regionally tailored gene deployment. Author summary: Breeding for disease resistant cultivars that withstand pathogen infection represents an important strategy for environmentally sustainable wheat production. The underlying disease resistance genes however vary greatly in their efficacy and durability against fast evolving fungal pathogens such as wheat powdery mildew. Pathogens evade recognition by immune receptors through mutation or loss of recognized avirulence effector proteins, resulting in local or global breakdown of resistance genes. To improve the durability of resistance genes and allow for efficient regional deployment of resistance sources, pathogen-informed strategies that rely on avirulence effector identification, characterization and monitoring are therefore crucial. Here, we describe a new approach for rapid identification of avirulence effectors in the wheat powdery mildew pathogen: the AD assay. We show that the AD assay reduces time and costs compared to previous approaches, while simultaneously allowing candidate gene identification with high precision. We deploy the AD assay to identify the avirulence effector AvrPm60 recognized by the wheat immune receptor Pm60 and characterize the prerequisites of Pm60-mediated resistance. Our study shows how rapid avirulence effector identification can contribute to a detailed understanding of the interplay between avirulence effectors and resistance genes and can thus guide future breeding decisions. [ABSTRACT FROM AUTHOR]

The regulation of virulence in plant-pathogenic fungi has emerged as a key area of importance underlying host infections. Recent work has highlighted individual transcription factors (TFs) that serve important roles. A prominent example is PnPf2, a member of the Zn2Cys6 family of fungal TFs, which controls the expression of effectors and other virulence-associated genes in Parastagonospora nodorum during infection of wheat. PnPf2 orthologues are similarly important for other major fungal pathogens during infection of their respective host plants, and have also been shown to control polysaccharide metabolism in model saprophytes. In each case, the direct genomic targets and associated regulatory mechanisms were unknown. Significant insight was made here by investigating PnPf2 through chromatin-immunoprecipitation (ChIP) and mutagenesis approaches in P. nodorum. Two distinct binding motifs were characterised as positive regulatory elements and direct PnPf2 targets identified. These encompass known effectors and other components associated with the P. nodorum pathogenic lifestyle, such as carbohydrate-active enzymes and nutrient assimilators. The results support a direct involvement of PnPf2 in coordinating virulence on wheat. Other prominent PnPf2 targets included TF-encoding genes. While novel functions were observed for the TFs PnPro1, PnAda1, PnEbr1 and the carbon-catabolite repressor PnCreA, our investigation upheld PnPf2 as the predominant transcriptional regulator characterised in terms of direct and specific coordination of virulence on wheat, and provides important mechanistic insights that may be conserved for homologous TFs in other fungi. Author summary: Fungal pathogens cause large crop losses worldwide and consequently much attention has focused on improving host genetic resistance to diseases. These pathogens use effectors, which require coordinated expression at specific stages of the pathogenic lifecycle, to manipulate the host plant metabolism in favour of infection. However, our understanding of the underlying regulatory components, their direct interactions and their evolutionary origins is lacking. The Pf2 TF-orthologue family underpins virulence and effector gene expression in several fungal phytopathogens, including Parastagonospora nodorum. This study provided significant insight into the DNA-binding regulatory mechanisms of P. nodorum PnPf2, as well as further evidence for its important role in regulating virulence. In the context of crop protection, the Pf2 TFs present opportune targets in major fungal pathogens to screen for direct or indirect inhibitor compounds to suppress virulence and improve disease resistance. [ABSTRACT FROM AUTHOR]

The fungus Parastagonospora nodorum causes septoria nodorum blotch on wheat. The role of the fungal Velvet-family transcription factor VeA in P. nodorum development and virulence was investigated here. Deletion of the P. nodorum VeA ortholog, PnVeA, resulted in growth abnormalities including pigmentation, abolished asexual sporulation and highly reduced virulence on wheat. Comparative RNA-Seq and RT-PCR analyses revealed that the deletion of PnVeA also decoupled the expression of major necrotrophic effector genes. In addition, the deletion of PnVeA resulted in an up-regulation of four predicted secondary metabolite (SM) gene clusters. Using liquid-chromatography mass-spectrometry, it was observed that one of the SM gene clusters led to an accumulation of the mycotoxin alternariol. PnVeA is essential for asexual sporulation, full virulence, secondary metabolism and necrotrophic effector regulation. [ABSTRACT FROM AUTHOR]

Septoria nodorum blotch (SNB) and tan spot, caused by the necrotrophic fungal pathogens Parastagonospora nodorum and Pyrenophora tritici-repentis, respectively, often occur together as a leaf spotting disease complex on wheat (Triticum aestivum L.). Both pathogens produce necrotrophic effectors (NEs) that contribute to the development of disease. Here, genome-wide association analysis of a diverse panel of 264 winter wheat lines revealed novel loci on chromosomes 5A and 5B associated with sensitivity to the NEs SnTox3 and SnTox5 in addition to the known sensitivity genes for NEs Ptr/SnToxA, SnTox1, SnTox3, and SnTox5. Sensitivity loci for SnTox267 and Ptr ToxB were not detected. Evaluation of the panel with five P. nodorum isolates for SNB development indicated the Snn3-SnTox3 and Tsn1-SnToxA interactions played significant roles in disease development along with additional QTL on chromosomes 2A and 2D, which may correspond to the Snn7-SnTox267 interaction. For tan spot, the Tsc1-Ptr ToxC interaction was associated with disease caused by two isolates, and a novel QTL on chromosome 7D was associated with a third isolate. The Tsn1-ToxA interaction was associated with SNB but not tan spot. Therefore some, but not all, of the previously characterized host gene-NE interactions in these pathosystems play significant roles in disease development in winter wheat. Based on these results, breeders should prioritize the selection of resistance alleles at the Tsc1, Tsn1, Snn3, and Snn7 loci as well as the 2A and 7D QTL to obtain good levels of resistance to SNB and tan spot in winter wheat. [ABSTRACT FROM AUTHOR]

Under intense breeding, modern wheats, such as durum (Triticum turgidum L. ssp. durum), are believed to have lost nutritional quality and protein content while increasing productivity. Emmer (Triticum turgidum ssp. dicoccum Thell) and wild emmer (Triticum turgidum ssp. dicoccoides) are alternative resources for breeding programs by offering favorable alleles to be introgressed into modern materials and thus broadening their genetic diversity. Studies conducted so far have shown that durum wheat has better performance in agronomical qualities and protein quality than T. dicoccum and T. dicoccoides. However, its grain protein content (GPC) and Fe/Zn concentrations are lower. Several QTL for yield, GPC, and nutrient content in T. dicoccoides have been described, demonstrating its potential for transfer of important genes such as Gpc-B1 into modern cultivars. The Gpc-B1 gene increased the grain protein and Fe and Zn contents, but the agronomic performance of some of the modern recipients was reduced. Understanding the correlations and relationships between agronomic, chemical, and nutritional qualities would simplify selection through breeding for a single trait. Combining this knowledge with conventional breeding, MAS, and new breeding techniques would facilitate the QTL studies in these ancestral wheats and the development of new durum cultivars while retaining the agronomic qualities. In this review, we compare some grain parameters of T. durum, T. dicoccum, and T. dicoccoides wheats, including Fe and Zn content and their genetic aspects, and the existing information is analyzed and integrated for the future prospects of durum wheat improvement. [ABSTRACT FROM AUTHOR]

Key message: Genetic characterization of a major spot form net blotch susceptibility locus to using linkage mapping to identify a candidate gene and user-friendly markers in barley. Spot form net blotch (SFNB), caused by the necrotrophic fungal pathogen Pyrenophora teres f. maculata (Ptm), is an economically important foliar diseases in barley. Although various resistance loci have been identified, breeding for SFNB-resistant varieties has been hampered due to the complex virulence profile of Ptm populations. One resistance locus in the host may be effective against one specific isolate, but it may confer susceptibility to other isolates. A major susceptibility QTL on chromosome 7H, named Sptm1, was consistently identified in many studies. In the present study, we conduct fine mapping to localize Sptm1 with high resolution. A segregating population was developed from selected F2 progenies of the cross Tradition (S) × PI 67381 (R), in which the disease phenotype was determined by the Sptm1 locus alone. Disease phenotypes of critical recombinants were confirmed in the following two consecutive generations. Genetic mapping anchored the Sptm1 gene to an ⁓400 kb region on chromosome 7H. Gene prediction and annotation identified six protein-coding genes in the delimited Sptm1 region, and the gene encoding a putative cold-responsive protein kinase was selected as a strong candidate. Therefore, providing fine localization and candidate of Sptm1 for functional validation, our study will facilitate the understanding of susceptibility mechanism underlying the barley-Ptm interaction and offers a potential target for gene editing to develop valuable materials with broad-spectrum resistance to SFNB. [ABSTRACT FROM AUTHOR]

The advancement of precision engineering for crop trait improvement is important in the face of rapid population growth, climate change, and disease. To this end, targeted double-stranded break technology using RNAguided Cas9 has been adopted widely for genome editing in plants. Agrobacterium or particle bombardment-based delivery of plasmids encoding Cas9 and guide RNA (gRNA) is common, but requires optimization of expression and often results in random integration of plasmid DNA into the plant genome. Recent advances have described gene editing by the delivery of Cas9 and gRNA as pre-assembled ribonucleoproteins (RNPs) into various plant tissues, but with moderate efficiency in resulting regenerated plants. In this report we describe significant improvements to Cas9-RNP mediated gene editing in wheat. We demonstrate that Cas9-RNP assays in protoplasts are a fast and effective tool for rational selection of optimal gRNAs for gene editing in regenerable immature embryos (IEs), and that high temperature treatment enhances gene editing rates in both tissue types. We also show that Cas9- mediated editing persists for at least 14 days in gold particle bombarded wheat IEs. The regenerated edited wheat plants in this work are recovered at high rates in the absence of exogenous DNA and selection. With this method, we produce knockouts of a set of three homoeologous genes and two pathogenic effector susceptibility genes, engineering insensitivity to corresponding necrotrophic effectors produced by Parastagonospora nodorum. The establishment of highly efficient, exogenous DNA-free gene editing technology holds promise for accelerated trait diversity production in an expansive array of crops. [ABSTRACT FROM AUTHOR]

Key message: A new QTL for SNB, QSnb.nmbu-2AS, was found in both winter and spring wheat panels that can greatly advance SNB resistance breeding Septoria nodorum blotch (SNB), caused by the necrotrophic fungal pathogen Parastagonospora nodorum, is the dominant leaf blotch pathogen of wheat in Norway. Resistance/susceptibility to SNB is a quantitatively inherited trait, which can be partly explained by the interactions between wheat sensitivity loci (Snn) and corresponding P. nodorum necrotrophic effectors (NEs). Two Nordic wheat association mapping panels were assessed for SNB resistance in the field over three to four years: a spring wheat and a winter wheat panel (n = 296 and 102, respectively). Genome-wide association studies found consistent SNB resistance associated with quantitative trait loci (QTL) on eleven wheat chromosomes, and ten of those QTL were common in the spring and winter wheat panels. One robust QTL on the short arm of chromosome 2A, QSnb.nmbu-2AS, was significantly detected in both the winter and spring wheat panels. For winter wheat, using the four years of SNB field severity data in combination with five years of historical data, the effect of QSnb.nmbu-2AS was confirmed in seven of the nine years, while for spring wheat, the effect was confirmed for all tested years including the historical data from 2014 to 2015. However, lines containing the resistant haplotype are rare in both Nordic spring (4.0%) and winter wheat cultivars (15.7%), indicating the potential of integrating this QTL in SNB resistance breeding programs. In addition, clear and significant additive effects were observed by stacking resistant alleles of the detected QTL, suggesting that marker-assisted selection can greatly facilitate SNB resistance breeding. [ABSTRACT FROM AUTHOR]

Septoria nodorum blotch (SNB) is a foliar disease of wheat caused by the necrotrophic fungal pathogen Parastagonospora nodorum. Research over the last two decades has shown that the wheat-P. nodorum pathosystem mostly follows an inverse gene-for-gene model. The fungus produces necrotrophic effectors (NEs) that interact with specific host gene products encoded by dominant sensitivity (S) genes. When a compatible interaction occurs, a 'defense response' in the host leads to programmed cell death thereby provided dead/dying cells from which the pathogen, being a necrotroph, can acquire nutrients allowing it to grow and sporulate. To date, nine S gene-NE interactions have been characterized in this pathosystem. Five NE-encoding genes, SnTox1, SnTox3, SnToxA, SnTox5, and SnTox267, have been cloned along with three host S genes, Tsn1, Snn1, and Snn3-D1. Studies have shown that P. nodorum hijacks multiple and diverse host targets to cause disease. SNB resistance is often quantitative in nature because multiple compatible interactions usually occur concomitantly. NE gene expression plays a key role in disease severity, and the effect of each compatible interaction can vary depending on the other existing compatible interactions. Numerous SNB-resistance QTL have been identified in addition to the known S genes, and more research is needed to understand the nature of these resistance loci. Marker-assisted elimination of S genes through conventional breeding practices and disruption of S genes using gene editing techniques are both effective strategies for the development of SNB-resistant wheat cultivars, which will become necessary as the global demand for sustenance grows. [ABSTRACT FROM AUTHOR]

Understanding biotic changes that occur alongside climate change constitute a research priority of global significance. Here, we address a plant pathogen that poses a serious threat to life on natural oases, where climate change is already taking a toll and severely impacting human subsistence. Fusarium oxysporum f. sp. albedinis is a pathogen that causes dieback disease on date palms, a tree that provides several critical ecosystem services in natural oases; and consequently, of major importance in this vulnerable habitat. Here, we assess the current state of global pathogen spread, we annotate the genome of a sequenced pathogen strain isolated from the native range and we analyse its in silico secretome. The palm dieback pathogen secretes a large arsenal of effector candidates including a variety of toxins, a distinguished profile of secreted in xylem proteins (SIX) as well as an expanded protein family with an N-terminal conserved motif [SG]PC[KR]P that could be involved in interactions with host membranes. Using agrobiodiversity as a strategy to decrease pathogen infectivity, while providing short term resilient solutions, seems to be widely overcome by the pathogen. Hence, the urgent need for future mechanistic research on the palm dieback disease and a better understanding of pathogen genetic diversity. [ABSTRACT FROM AUTHOR]

The fungus Parastagonospora nodorum uses proteinaceous necrotrophic effectors (NEs) to induce tissue necrosis on wheat leaves during infection, leading to the symptoms of septoria nodorum blotch (SNB). The NEs Tox1 and Tox3 induce necrosis on wheat possessing the dominant susceptibility genes Snn1 and Snn3B1/Snn3D1, respectively. We previously observed that Tox1 is epistatic to the expression of Tox3 and a quantitative trait locus (QTL) on chromosome 2A that contributes to SNB resistance/susceptibility. The expression of Tox1 is significantly higher in the Australian strain SN15 compared to the American strain SN4. Inspection of the Tox1 promoter region revealed a 401 bp promoter genetic element in SN4 positioned 267 bp upstream of the start codon that is absent in SN15, called PE401. Analysis of the world-wide P. nodorum population revealed that a high proportion of Northern Hemisphere isolates possess PE401 whereas the opposite was observed in representative P. nodorum isolates from Australia and South Africa. The presence of PE401 removed the epistatic effect of Tox1 on the contribution of the SNB 2A QTL but not Tox3. PE401 was introduced into the Tox1 promoter regulatory region in SN15 to test for direct regulatory roles. Tox1 expression was markedly reduced in the presence of PE401. This suggests a repressor molecule(s) binds PE401 and inhibits Tox1 transcription. Infection assays also demonstrated that P. nodorum which lacks PE401 is more pathogenic on Snn1 wheat varieties than P. nodorum carrying PE401. An infection competition assay between P. nodorum isogenic strains with and without PE401 indicated that the higher Tox1-expressing strain rescued the reduced virulence of the lower Tox1-expressing strain on Snn1 wheat. Our study demonstrated that Tox1 exhibits both 'selfish' and 'altruistic' characteristics. This offers an insight into a complex NE-NE interaction that is occurring within the P. nodorum population. The importance of PE401 in breeding for SNB resistance in wheat is discussed. Author summary: Breeding for durable resistance to fungal diseases in crops is a continual challenge for crop breeders. Fungal pathogens evolve ways to overcome host resistance by masking themselves through effector evolution and evasion of broad-spectrum defense responses. Association studies on mapping populations infected by isolate mixtures are often used by researchers to seek out novel sources of genetic resistance. Disease resistance quantitative trait loci (QTL) are often minor or inconsistent across environments. This is a particular problem with septoria diseases of cereals such as septoria nodorum blotch (SNB) of wheat caused by Parastagonospora nodorum. The fungus uses a suite of necrotrophic effectors (NEs) to cause SNB. We characterised a genetic element, called PE401, in the promoter of the major NE gene Tox1, which is present in some P. nodorum isolates. PE401 functions as a transcriptional repressor of Tox1 and exerts epistatic control on another major SNB resistance QTL in the host. In the context of crop protection, constant surveillance of the pathogen population for the frequency of PE401 in conjunction with NE diversity will enable agronomists to provide the best advice to growers on which wheat varieties can be tailored to provide optimal SNB resistance to regional pathogen population genotypes. [ABSTRACT FROM AUTHOR]

This article is a Commentary on Kariyawasam et al. (2022), 233: 409–426 and Richards et al. (2022), 233: 427–442. [ABSTRACT FROM AUTHOR]

Summary: Parastagonospora nodorum is an economically important necrotrophic fungal pathogen of wheat. Parastagonospora nodorum secretes necrotrophic effectors that target wheat susceptibility genes to induce programmed cell death (PCD). In this study, we cloned and functionally validated SnTox5 and characterized its role in pathogenesis.We used whole genome sequencing, genome‐wide association study (GWAS) mapping, CRISPR‐Cas9‐based gene disruption, gain‐of‐function transformation, quantitative trait locus (QTL) analysis, haplotype and isoform analysis, protein modeling, quantitative PCR, and laser confocal microscopy to validate SnTox5 and functionally characterize SnTox5.SnTox5 is a mature 16.26 kDa protein with high structural similarity to SnTox3. Wild‐type and mutant P. nodorum strains and wheat genotypes of SnTox5 and Snn5, respectively, were used to show that SnTox5 not only targets Snn5 to induce PCD but also facilitates the colonization of the mesophyll layer even in the absence of Snn5.Here we show that SnTox5 facilitates the efficient colonization of the mesophyll tissue and elicits PCD specific to host lines carrying Snn5. The homology to SnTox3 and the ability of SnTox5 to facilitate the colonizing of the mesophyll also suggest a role in the suppression of host defense before PCD induction. See also the Commentary on this article by Kanyuka et al., 233: 11–14. [ABSTRACT FROM AUTHOR]

Summary: Parastagonospora nodorum is a fungal pathogen of wheat. As a necrotrophic specialist, it deploys effector proteins that target dominant host susceptibility genes to elicit programmed cell death (PCD). Here we identify and functionally validate the effector targeting the host susceptibility genes Snn2, Snn6 and Snn7.We utilized whole‐genome sequencing, association mapping, gene‐disrupted mutants, gain‐of‐function transformants, virulence assays, bioinformatics and quantitative PCR to characterize these interactions.A single proteinaceous effector, SnTox267, targeted Snn2, Snn6 and Snn7 to trigger PCD. Snn2 and Snn6 functioned cooperatively to trigger PCD in a light‐dependent pathway, whereas Snn7‐mediated PCD functioned in a light‐independent pathway. Isolates harboring 20 SnTox267 protein isoforms quantitatively varied in virulence. The diversity and distribution of isoforms varied between populations, indicating adaptation to local selection pressures. SnTox267 deletion resulted in the upregulation of effector genes SnToxA, SnTox1 and SnTox3.We validated a novel effector operating in an inverse‐gene‐for‐gene manner to target three genetically distinct host susceptibility genes and elicit PCD. The discovery of the complementary gene action of Snn2 and Snn6 indicates their potential function in a guard or decoy model. Additionally, differences in light dependency in the elicited pathways and upregulation of unlinked effectors sheds new light onto a complex fungal necrotroph–host interaction. See also the Commentary on this article by Kanyuka et al., 233: 11–14. [ABSTRACT FROM AUTHOR]

Key message: Two major and stable QTLs for spike compactness and length were detected and validated in multiple genetic backgrounds and environments, and their pleiotropic effects on yield-related traits were analyzed. Spike compactness (SC) and length (SL) are greatly associated with wheat (Triticum aestivum L.) grain yield. To detect quantitative trait loci (QTL) associated with SC and SL, two biparental populations derived from crosses of Chuanmai42/Kechengmai1 and Chuanmai42/Chuannong16 were employed to perform QTL mapping in five environments. A total of 34 QTLs were identified, in which six major QTLs were repeatedly detected in more than four environments and the best linear unbiased prediction datasets, explaining 7.13–33.6% of phenotypic variation. These major QTLs were co-located in two genomic regions on chromosome 5A and 6A, namely QSc/Sl.cib-5A and QSc/Sl.cib-6A, respectively. By developing kompetitive allele-specific PCR (KASP) markers that linked to them, the two loci were validated in different genetic backgrounds, and their interactions were also analyzed. Comparison analysis showed that QSc/Sl.cib-5A was not Vrn-A1 and Q, and QSc/Sl.cib-6A was likely a new locus for SC and SL. Both QSc/Sl.cib-5A and QSc/Sl.cib-6A had pleiotropic effects on other yield-related traits including plant height, thousand grain weight and grain length. Therefore, the two loci combined with the developed KASP markers might be potentially applicable in wheat breeding. Furthermore, based on the spatiotemporal expression patterns, gene annotation, orthologous search and sequence differences, TraesCS5A01G301400 and TraesCS6A01G090300 were considered as potential candidates for QSc/Sl.cib-5A and QSc/Sl.cib-6A, respectively. These results provided valuable information for fine mapping and cloning of the two loci in the future. [ABSTRACT FROM AUTHOR]

Emmer wheat (Triticum turgidum ssp. dicoccum) is an important gene source for wheat improvement but less studied in crosses with its descendant species durum (Triticum turgidum ssp. durum), especially in respect to the type of genetic components, intergenic interactions and the genetic mechanisms governing responses to drought. In this study, generation means analysis was performed using F1, F2, BC1P1 and BC1P2 from two different crosses of emmer × durum. Seeds were planted in a RCBD design with three replications under two water regimes. Results showed that there was a highly considerable difference between generations for all studied traits. The presence of significant mean parameter for all the traits, indicated the quantitative inheritance of the traits. Estimating the number of effective genes, polygenic control of the traits were confirmed. In moisture stress condition, epistatic effect for grain yield and yield-related traits illustrated the importance of epistasis in plant adaptation and performance stability. The additive × additive effect, which is fixable, was remarkable in both crosses. Under both water regimes, narrow-sense heritability was relatively high and estimates of gain from selection were positive for most of the traits. Among generations studied, the backcrosses were superior for drought tolerant indices. Based on the results, emmer wheat seems to have genetic potential for durum improvement. Pasta is mainly produced from durum wheat (Triticum turgidum ssp. durum , which is different from bread wheat (Triticum aestivum L.). To make durum wheat grow and yield in water limited regions of the world, drought tolerant genes may be transferred from a relative species emmer wheat (Triticum turgidum ssp. dicoccum). This research was conducted to make this achievable by understanding how well the gens between the two species combine and express themselves. [ABSTRACT FROM AUTHOR]

Summary: Plant pathogens cause disease through secreted effector proteins, which act to promote infection. Typically, the sequences of effectors provide little functional information and further targeted experimentation is required. Here, we utilized a structure/function approach to study SnTox3, an effector from the necrotrophic fungal pathogen Parastagonospora nodorum, which causes cell death in wheat‐lines carrying the sensitivity gene Snn3.We developed a workflow for the production of SnTox3 in a heterologous host that enabled crystal structure determination and functional studies. We show this approach can be successfully applied to study effectors from other pathogenic fungi.The β‐barrel fold of SnTox3 is a novel fold among fungal effectors. Structure‐guided mutagenesis enabled the identification of residues required for Snn3 recognition. SnTox3 is a pre‐pro‐protein, and the pro‐domain of SnTox3 can be cleaved in vitro by the protease Kex2. Complementing this, an in silico study uncovered the prevalence of a conserved motif (LxxR) in an expanded set of putative pro‐domain‐containing fungal effectors, some of which can be cleaved by Kex2 in vitro.Our in vitro and in silico study suggests that Kex2‐processed pro‐domain (designated here as K2PP) effectors are common in fungi and this may have broad implications for the approaches used to study their functions. [ABSTRACT FROM AUTHOR]

Background: Threshability, rachis fragility and spike shape are critical traits for the domestication and evolution of wheat, determining the crop yield and efficiency of the harvest. Spelt factor gene Q controls a wide range of domestication-related traits in polyploid wheats, including those mentioned above. The main goal of the present study was to characterise the Q gene for uninvestigated accessions of wheats, including four endemics, and Aegilops accessions, and to analyze the species evolution based on differences in Q gene sequences. Results: We have studied the spike morphology for 15 accessions of wheat species, including four endemics, namely Triticum macha, T. tibetanum, T. aestivum ssp. petropavlovskyi and T. spelta ssp. yunnanense, and 24 Aegilops accessions, which are donors of B and D genomes for polyploid wheat. The Q-5A, q-5D and q-5S genes were investigated, and a novel allele of the Q-5A gene was found in accessions of T. tibetanum (KU510 and KU515). This allele was similar to the Q allele of T. aestivum cv. Chinese Spring but had an insertion 161 bp in length within exon 5. This insertion led to a frameshift and premature stop codon formation. Thus, the T. tibetanum have spelt spikes, which is probably determined by the gene Tg, rather than Q. We determined the variability within the q-5D genes among hexaploid wheat and their D genome donor Aegilops tauschii. Moreover, we studied the accessions C21–5129, KU-2074, and K-1100 of Ae. tauschii ssp. strangulata, which could be involved in the origin of hexaploid wheats. Conclusions: The variability and phylogenetic relationships of the Q gene sequences studied allowed us to clarify the relationships between species of the genus Triticum and to predict the donor of the D genome among the Ae. tauschii accessions. Ae. tauschii ssp. strangulata accessions C21–5129, KU-2074 and K-1100 are the most interesting among the analysed accessions, since their partial sequence of q-5D is identical to the q-5D of T. aestivum cv. Chinese Spring. This result indicates that the donor is Ae. tauschii ssp. strangulata but not Ae. tauschii ssp. tauschii. Our analysis allowed us to clarify the phylogenetic relationships in the genus Triticum. [ABSTRACT FROM AUTHOR]

Key message: Two stem rust resistance genes identified on chromosome arms 2BL and 6AL of the cultivated emmer wheat accession PI 193883 can be used for protecting modern varieties against Ug99 strains. The wheat research community consistently strives to identify new genes that confer resistance to stem rust caused by the fungal pathogen Puccinia graminis f. sp. tritici Eriks & E. Henn (Pgt). In the current study, our objective was to identify and genetically characterize the stem rust resistance derived from the cultivated emmer accession PI 193883. A recombinant inbred line population developed from a cross between the susceptible durum wheat line Rusty and PI 193883 was genotyped and evaluated for reaction to Pgt races TTKSK, TRTTF, and TMLKC. Two QTLs conferring resistance were identified on chromosome arms 2BL (QSr.fcu-2B) and 6AL (QSr.fcu-6A). The stem rust resistance gene (Sr883-2B) underlying QSr.fcu-2B was recessive, and based on its physical location it is located proximal to the Sr9 region. QSr.fcu-6A was located in the Sr13 region, but PI 193883 is known to carry the susceptible haplotype S4 for Sr13, indicating that the gene underlying QSr.fcu-6A (Sr883-6A) is likely a new allele of Sr13 or a gene residing close to Sr13. Three IWGSC scaffold-based simple sequence repeat (SSR) and two SNP-based semi-thermal asymmetric reverse PCR (STARP) markers were developed for the Sr883-2B region, and one STARP marker was developed for Sr883-6A. Sr883-2B was epistatic to Sr883-6A for reaction to TTKSK and TRTTF, and the two genes had additive effects for TMLKC. These two genes and the markers developed in this research provide additional resources and tools for the improvement in stem rust resistance in durum and common wheat breeding programs. [ABSTRACT FROM AUTHOR]