Tan Spot Research Articles

Racial composition and variability of the <i>ToxA</i> gene in geographically distant populations of <i>Pyrenophora tritici-repentis</i>

Pyrenophora tritici-repentis causing the tan spot of wheat produces specific necrotrophic effectors Ptr ToxA, Ptr ToxB and Ptr ToxC, inducing necrosis and chlorosis on the leaves of susceptible varieties. Based on the ability of P. tritici-repentis strains to produce specific necrotrophic effectors or their combinations, the eight races of the pathogen are distinguished. Monitoring the race composition of P. tritici-repentis populations is necessary to assess the evolutionary potential of the pathogen and develop a methodology for breeding wheat cultivars with long-term resistance. We analyzed 179 monoconidial P. tritici-repentis strains from Kazakhstan and Russia populations in 2020–2022. The widespread distribution of races 2 and 4 was revealed, strains of which were present in each analyzed P. tritici-repentis population with a frequency of 2–36% and 7–82%, respectively. The dominance of avirulent race 4 was noted: the strains of this race accounted for 27% of all analyzed P. tritici-repentis strains. Molecular identification of the ToxA and ToxB genes, as well as toxb, a homolog of the ToxB gene, in 118 P. tritici-repentis strains from six populations revealed the presence of the ToxA gene in 69% of the analyzed strains. The ToxB gene was not detected in any strains, while the toxb gene was found sporadically and was identified in the genome of 18 P. tritici-repentis strains (9%), most of which were avirulent and belonged to race 4. In PCR with specific primers for ToxA gene of ten P. tritici-repentis strains a product of ≈ 800 bp was amplified, which turned out to be significantly larger than expected. This was explained by the presence of an insertion in the amplified region of the ToxA gene. All P. tritici-repentis strains with the ToxAL were assigned to races 4 and 5, which do not form the necrotrophic effector Ptr ToxA. The structure of the ToxAL gene and its protein product is the subject of further research.

Discovery of Two Novel Phthalide Phytotoxins from the Wheat Tan Spot Fungal Pathogen Pyrenophora tritici-repentis.

The Dothideomycete fungal pathogen Pyrenophora tritici-repentis (Ptr) is the causal agent of the tan spot disease of wheat. The proteinaceous necrotrophic effectors ToxA and ToxB are well characterized. A nonproteinaceous effector called ToxC has also been partially characterized. Ptr produces a number of other small molecular weight compounds, but these remain poorly characterized. In this study, two novel compounds, designated ToxE1 and ToxE2, capable of inducing chlorotic symptoms on wheat leaves in a cultivar-specific manner, were purified from Ptr liquid cultures. There is no evidence that these compounds correspond to ToxC. Most isolates produced ToxE1, ToxE2, or both, and both compounds were detected in infected wheat leaves. The structures of both analogues were elucidated by NMR spectroscopy and comprise a phthalide core structure with an amide moiety. We postulate that these compounds have a general phytotoxic effect and may have an ancillary role in disease development.

Crop Density and Sowing Timing Effect on Tan Spot Occurrence in Spring Wheat

Tan spot (Pyrenophora tritici-repentis) is presenting a persistent challenge to the plant health and yield of all wheat-growing regions. This research is focused on tan spot disease management in spring wheat when planted at three distinct times and with three different seeding rates without the use of fungicides. Across all years, higher seed rates (500 and 600 seeds per m2) generally resulted in lower tan spot intensity compared to the lower seed rate (400 seeds per m2). Significant differences in tan spot intensity were observed across seed rates at all sowing times. In 2021, the percentage of the AUDPC was significantly higher in the late sowing time (324.58%), with about a 2-fold difference compared with the early (167.48%) and optimal sowing time (191.80%). This suggests that delayed sowing significantly exacerbates disease occurrence. The combined effect of sowing time and year on the AUDPC was notably significant. The AUDPC of the tan spot in all seed rates was the highest in the late sowing time plots in comparison to the ideal and initial planting dates plots. Our results demonstrate how important seed rate and sowing timing are in determining the degree of tan spot in spring wheat. Growing crop methods may be improved by taking these elements into account to better control tan spots. More agricultural methods and environmental aspects should be investigated in future studies to create all-encompassing tan spot control plans.

Association mapping of tan spot and septoria nodorum blotch resistance in cultivated emmer wheat.

A total of 65 SNPs associated with resistance to tan spot and septoria nodorum blotch were identified in a panel of 180 cultivated emmer accessions through association mapping Tan spot and septoria nodorum blotch (SNB) are foliar diseases caused by the respective fungal pathogens Pyrenophora tritici-repentis and Parastagonospora nodorum that affect global wheat production. To find new sources of resistance, we evaluated a panel of 180 cultivated emmer wheat (Triticum turgidum ssp. dicoccum) accessions for reactions to four P. tritici-repentis isolates Pti2, 86-124, 331-9 and DW5, two P. nodorum isolate, Sn4 and Sn2000, and four necrotrophic effectors (NEs) produced by the pathogens. About 8-36% of the accessions exhibited resistance to the four P. tritici-repentis isolates, with five accessions demonstrating resistance to all isolates. For SNB, 64% accessions showed resistance to Sn4, 43% to Sn2000 and 36% to both isolates, with Spain (11% accessions) as the most common origin of resistance. To understand the genetic basis of resistance, association mapping was performed using SNP (single nucleotide polymorphism) markers generated by genotype-by-sequencing and the 9K SNP Infinium array. A total of 46 SNPs were significantly associated with tan spot and 19 SNPs with SNB resistance or susceptibility. Six trait loci on chromosome arms 1BL, 3BL, 4AL (2), 6BL and 7AL conferred resistance to two or more isolates. Known NE sensitivity genes for disease development were undetected except Snn5 for Sn2000, suggesting novel genetic factors are controlling host-pathogen interaction in cultivated emmer. The emmer accessions with the highest levels of resistance to the six pathogen isolates (e.g., CItr 14133-1, PI 94634-1 and PI 377672) could serve as donors for tan spot and SNB resistance in wheat breeding programs.

The wheat tan spot pathosystem in Australia: A showcase of effector‐assisted breeding

AbstractTan spot disease of wheat (also known as yellow spot) is caused by the necrotrophic fungal pathogen Pyrenophora tritici‐repentis (Ptr). Initially described as a grass pathogen, Ptr has become a wheat pathogen of global importance. In Australia, tan spot was first recorded in 1952 as a minor wheat disease. However, by the 1970s tan spot had reached epidemic levels in Australia with yield losses of up to 49% reported in the north‐eastern region. A national survey carried out in 2007/2008 placed tan spot as the most economically important wheat disease with an estimated yield loss of 6%, corresponding to nearly a quarter of all disease losses. The incidence of tan spot in Australia has now markedly reduced with some wheat breeding programmes no longer considering tan spot disease resistance to be a priority trait. The disease can be effectively managed with integrated control strategies such as crop rotation, timely application of fungicides and removal of surface stubble. However, the key to the success of controlling tan spot disease in Australia has been achieved through wheat breeding programmes. The development of tan spot resistance resources suitable for the Australian climate was a concerted effort between national and international research organizations and Australian wheat breeders, supported by the Australian Grains Research Development Corporation (GRDC). While traditional breeding was essential to combat the disease, this article highlights the value of effector biology in assisting the development of resistant cultivars.

Nitrogen and Silicon Contribute to Wheat Defense's to Pyrenophora tritici-repentis, but in an Independent Manner.

Nitrogen (N) and silicon (Si) are mineral elements that have shown a reduction in the damage caused by tan spot (Pyrenophora tritici-repentis (Ptr)) in wheat. However, the effects of these elements were studied separately, and the N and Si interaction effect on wheat resistance to tan spot remains elusive. Histocytological and biochemical defense responses against Ptr in wheat leaves treated with Si (+Si) at low (LN) and high N (HN) inputs were investigated. Soil amendment with Si reduced the tan spot severity in 18% due to the increase in the leaf Si concentration (around 30%), but it was affected by the N level used. The superoxide dismutase (SOD) activity was higher in +Si plants and inoculated with Ptr, leading to early and higher H2O2 and callose accumulation in wheat leaf. Interestedly, phenylalanine ammonia-lyase (PAL) activity was induced by the Si supplying, being negatively affected by the HN rate. Meanwhile, catalase (CAT), and peroxidase (POX) activities showed differential response patterns according to the Si and N rates used. Tan spot severity was reduced by both elements, but their interaction does not evidence synergic effects in this disease's control. Wheat plants from -Si and HN and +Si and LN treatments recorded lower tan spot severity.

Genomic prediction of synthetic hexaploid wheat upon tetraploid durum and diploid Aegilops parental pools.

Bread wheat (Triticum aestivum L.) is a globally important food crop, which was domesticated about 8-10,000 years ago. Bread wheat is an allopolyploid, and it evolved from two hybridization events of three species. To widen the genetic base in breeding, bread wheat has been re-synthesized by crossing durum wheat (Triticum turgidum ssp. durum) and goat grass (Aegilops tauschii Coss), leading to so-called synthetic hexaploid wheat (SHW). We applied the quantitative genetics tools of "hybrid prediction"-originally developed for the prediction of wheat hybrids generated from different heterotic groups - to a situation of allopolyploidization. Our use-case predicts the phenotypes of SHW for three quantitatively inherited global wheat diseases, namely tan spot (TS), septoria nodorum blotch (SNB), and spot blotch (SB). Our results revealed prediction abilities comparable to studies in 'traditional' elite or hybrid wheat. Prediction abilities were highest using a marker model and performing random cross-validation, predicting the performance of untested SHW (0.483 for SB to 0.730 for TS). When testing parents not necessarily used in SHW, combination prediction abilities were slightly lower (0.378 for SB to 0.718 for TS), yet still promising. Despite the limited phenotypic data, our results provide a general example for predictive models targeting an allopolyploidization event and a method that can guide the use of genetic resources available in gene banks.

LEVERAGING DEEP LEARNING FOR ACCURATE RICE LEAF DISEASE RECOGNITION

: Imagine a Rice Field, seemingly healthy, yet harboring invisible foes. This paper delves into the world of crop disease detection for the Tan spot, Leaf blight, Sheath decay, Bacterial leaf rot, and False smut Dataset consists of 3546 images. The image segmentation is done by BIRCH clustering followed by GMM clustering; various texture features have been extracted through this. The classification is done using existing models such as VGG16, VGG19, RESNET50, and INCEPTION V3. After comparing various models and validation, the observation was made that VGG19 performs well compared to other models. The overall accuracy obtained for the VGG19 is 95.88.%. The achieved accuracy surpasses that of conventional backpropagation neural network models, indicating significant advancements in crop disease diagnosis. This study introduces a novel approach that opens avenues for future research in the field of deep learning for crop disease diagnosis.

A New ToxA Haplotype in the Wheat Fungal Pathogen Bipolaris sorokiniana.

The necrotrophic effector ToxA is a well-studied virulence factor produced by several fungal necrotrophs. Initially cloned from the wheat tan spot pathogen Pyrenophora tritici-repentis in 1996, ToxA was found almost a decade later in another fungal pathogen, Parastagonospora nodorum, and its sister species, Parastagonospora pseudonodorum. In 2018, ToxA was detected in a third wheat fungal pathogenic species, Bipolaris sorokiniana, which causes spot blotch disease. However, unlike the case with P. tritici-repentis and P. nodorum, the ToxA in B. sorokiniana has only been investigated in recent years. In this report, five Australian B. sorokiniana isolates were assessed for the presence of ToxA. Four isolates were found to contain ToxA. While one isolate harbored the previously reported ToxA haplotype sequence (ToxA19), three isolates contain a different haplotype, designated herein as ToxA25, which has a nonsynonymous mutation resulting in an amino acid change of glycine to arginine at position 168. Both B. sorokiniana ToxA isoforms, when heterologously expressed in Escherichia coli, exhibited the classic ToxA necrosis-inducing activity on ToxA-sensitive Tsn1 cultivars. Preliminary analysis of the B. sorokiniana isolates in Australian wheat cultivars showed that isolates with ToxA19, ToxA25, or ToxA-deficient displayed various degrees of virulence, with the most aggressive isolates observed for those producing ToxA. Differences in spot blotch disease severity between Tsn1 and tsn1 cultivars were observed; however, this was not limited to the ToxA-producing isolates. The overall results suggest that the virulence of the Australian B. sorokiniana isolates is diverse, with the significance of ToxA-Tsn1 interactions depending on individual isolates.

Grain Yield and Quality Losses Caused by Tan Spot in Wheat Cultivars in Australia

Tan spot (TS), known in Australia as yellow leaf spot, is caused by the fungal pathogen Pyrenophora tritici-repentis, a major foliar disease of wheat. Four experiments were conducted between 2016 and 2017 in two different climatic zones of southeastern Australia to determine the impact of TS on grain yield and quality in six wheat cultivars with different resistance ratings. In each experiment, high and low TS disease scenarios were applied to each cultivar. Disease severity was assessed as either whole-plot percentage leaf area affected (%LAA) or top three leaf (flag to flag-2) %LAA. Whole-plot %LAA was analyzed using both repeated measurements and area under the disease progress curve (AUDPC). For whole-plot %LAA, the repeated measurements identified differences in epidemic progression at key growth stages not identified through AUDPC. Both AUDPC and end-of-season flag to flag-2 %LAA were negatively correlated with grain yield and screenings. Increased rainfall impacting disease development and number of rain days above 5 mm increased TS severity across both climatic zones. Cultivar resistance ratings influenced grain yield loss, with moderately resistant, moderately susceptible, and susceptible cultivars losing up to 6, 18, and 24% grain yield, respectively. High disease significantly increased screenings by up to 1, 3, and 5% for moderately resistant, moderately susceptible, and susceptible cultivars, respectively. This study demonstrated that TS can cause significant grain yield losses in southeastern Australia, and a minimum cultivar rating of moderate resistance to moderate susceptibility was required to prevent severe TS and associated grain yield and quality losses. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .

Evolution of the Toxb Gene in Pyrenophora tritici-repentis and Related Species.

Pyrenophora tritici-repentis (tan spot) is a destructive foliar pathogen of wheat with global impact. This ascomycete fungus possesses a highly plastic open pangenome shaped by the gain and loss of effector genes. This study investigated the allelic variations in the chlorosis-encoding gene ToxB across 422 isolates representing all identified pathotypes and worldwide origins. To gain better insights into ToxB evolution, we examined its presence and variability in other Pyrenophora spp. A ToxB haplotype network was constructed, revealing the evolutionary relationships of this gene (20 haplotypes) across four Pyrenophora species. Notably, toxb, the homolog of ToxB, was detected for the first time in the barley pathogen Pyrenophora teres. The ToxB/toxb genes display evidence of selection that is characterized by loss of function, duplication, and diverse mutations. Within the ToxB/toxb open reading frame, 72 mutations were identified, including 14 synonymous, 55 nonsynonymous, and 3 indel mutations. Remarkably, a, ∼5.6-kb Copia-like retrotransposon, named Copia-1_Ptr, was found inserted in the toxb gene of a race 3 isolate. This insert disrupted the ToxB gene's function, a first case of effector gene disruption by a transposable element in P. tritici-repentis. Additionally, a microsatellite with 25 nucleotide repeats (0 to 10) in the upstream region of ToxB suggested a potential mechanism influencing ToxB expression and regulation. Exploring ToxB-like protein distribution in other ascomycetes revealed the presence of ToxB-like proteins in 19 additional species, including the Leotiomycetes class for the first time. The presence/absence pattern of ToxB-like proteins defied species relatedness compared with a phylogenetic tree, suggesting a past horizontal gene transfer event during the evolution of the ToxB gene. [Formula: see text] Copyright © 2024 His Majesty the King in Right of Canada, as represented by the Minister of Agriculture and Agri-Food. This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Unraveling the dynamics of wheat leaf blight complex: isolation, characterization, and insights into pathogen population under Indian conditions.

Wheat, a staple food crop for 35% of the global population, faces a threat from Helminthosporium leaf blight (HLB), a complex of spot blotch (Bipolaris sorokiniana) and tan spot (Pyrenophora-tritici-repentis) diseases under warm and humid conditions. However, in Indian conditions, the knowledge of existing pathogen populations associated with the HLB complex is limited and largely dominated by only B. sorokiniana (spot blotch). To address this, diseased samples were collected from all six wheat growing zones during 2020-2022. The pathogenic species were identified through in-depth morphological characterization, supplemented with ITS-rDNA and GAPDH sequence analysis, a diagnostic SCAR marker, and pathogenicity studies on two wheat varieties: Sonalika and HD2733. The 32 isolates collected from 10 different states consist of B. spicifera (12.5% of all isolates), Exserohilum rostratum (9.3%), Bipolaris oryzae (3.1%), and B. sorokiniana (75%). B. sorokiniana exhibited the highest disease severity on both varieties. Other lesser-known pathogenic species also produced comparable disease severity as B. sorokiniana isolates and, therefore are economically important. Unraveling pathogen composition and biology aids in disease control and resistance breeding. Our study highlights economically impactful and lesser-known pathogenic species causing wheat leaf blight/spot blotch in India, guiding both current management and future resistance breeding strategies in plant pathology.

Modeling within and between Sub-Genomes Epistasis of Synthetic Hexaploid Wheat for Genome-Enabled Prediction of Diseases.

Common wheat (Triticum aestivum) is a hexaploid crop comprising three diploid sub-genomes labeled A, B, and D. The objective of this study is to investigate whether there is a discernible influence pattern from the D sub-genome with epistasis in genomic models for wheat diseases. Four genomic statistical models were employed; two models considered the linear genomic relationship of the lines. The first model (G) utilized all molecular markers, while the second model (ABD) utilized three matrices representing the A, B, and D sub-genomes. The remaining two models incorporated epistasis, one (GI) using all markers and the other (ABDI) considering markers in sub-genomes A, B, and D, including inter- and intra-sub-genome interactions. The data utilized pertained to three diseases: tan spot (TS), septoria nodorum blotch (SNB), and spot blotch (SB), for synthetic hexaploid wheat (SHW) lines. The results (variance components) indicate that epistasis makes a substantial contribution to explaining genomic variation, accounting for approximately 50% in SNB and SB and only 29% for TS. In this contribution of epistasis, the influence of intra- and inter-sub-genome interactions of the D sub-genome is crucial, being close to 50% in TS and higher in SNB (60%) and SB (60%). This increase in explaining genomic variation is reflected in an enhancement of predictive ability from the G model (additive) to the ABDI model (additive and epistasis) by 9%, 5%, and 1% for SNB, SB, and TS, respectively. These results, in line with other studies, underscore the significance of the D sub-genome in disease traits and suggest a potential application to be explored in the future regarding the selection of parental crosses based on sub-genomes.

Induced responses to the wheat pathogen: Tan Spot—(Pyrenophora tritici-repentis) in wheat (Triticum aestivum) focus on changes in defence associated and sugar metabolism

IntroductionTan Spot (TS) disease of wheat is caused by Pyrenophora tritici-repentis (Ptr), where most of the yield loss is linked to diseased flag leaves. As there are no fully resistant cultivars available, elucidating the responses of wheat to Ptr could inform the derivation of new resistant genotypes.ObjectivesThe study aimed to characterise the flag-leaf metabolomes of two spring wheat cultivars (Triticum aestivum L. cv. PF 080719 [PF] and cv. Fundacep Horizonte [FH]) following challenge with Ptr to gain insights into TS disease development.MethodsPF and FH plants were inoculated with a Ptr strain that produces the necrotrophic toxin ToxA. The metabolic changes in flag leaves following challenge (24, 48, 72, and 96 h post-inoculation [hpi]) with Ptr were investigated using untargeted flow infusion ionisation-high resolution mass spectroscopy (FIE-HRMS).ResultsBoth cultivars were susceptible to Ptr at the flag-leaf stage. Comparisons of Ptr- and mock-inoculated plants indicated that a major metabolic shift occurred at 24 hpi in FH, and at 48 hpi in PF. Although most altered metabolites were genotype specific, they were linked to common pathways; phenylpropanoid and flavonoid metabolism. Alterations in sugar metabolism as well as in glycolysis and glucogenesis pathways were also observed. Pathway enrichment analysis suggested that Ptr-triggered alterations in chloroplast and photosynthetic machinery in both cultivars, especially in FH at 96 hpi. In a wheat-Ptr interactome in integrative network analysis, “flavone and flavonol biosynthesis” and “starch and sucrose metabolism” were targeted as the key metabolic processes underlying PF–FH–Ptr interactions.ConclusionThese observations suggest the potential importance of flavone and flavonol biosynthesis as well as bioenergetic shifts in susceptibility to Ptr. This work highlights the value of metabolomic approaches to provide novel insights into wheat pathosystems.

Resistance of old winter bread wheat landraces to tan spot

Background. The most effective and environmentally safe way to combat wheat diseases is to produce cultivars resistant to their pathogens. For this purpose, old landraces are often used as genetically diverse sources of traits important for breeding. In the process of wheat breeding for resistance to tan spot caused by the fungus Pyrenophora tritici-repentis (Died.) Drechs. (abbr. Ptr), selection is carried out against the dominant allele of Tsn1, the gene of sensitivity to the toxin Ptr ToxA, which induces necrosis and represents the main pathogenicity factor of Ptr controlled by the ToxA gene. The aim of the study was to characterize a set of bread wheat (Triticum aestivum L.) accessions from the VIR collection for resistance to various Ptr populations, genotype these accessions using Xfcp623 – a DNA marker of the Tsn1 gene, and identify sources of tan spot resistance.Materials and methods. Sixty-seven accessions of winter bread wheat landraces were studied. Seedling resistance to two Ptr populations was assessed using a 5-point scale adopted at VIZR. The allelic state of Tsn1 was identified by PCR.Results. Dominant alleles of Tsn1 were found for 55% of the studied accessions. Seventeen accessions were resistant or moderately resistant to two Ptr populations and an isolate from Krasnodar Territory previously used for their characterization. Nine of them had the tsn1tsn1 genotype, and 8 had Tsn1Tsn1. The accessions mainly belonged to three agroecological groups proposed by N. I. Vavilov: “steppe winter bread wheat (Banatka wheats)”, “North European forest awnless bread wheats (Sandomirka wheats)”, and “Caucasian mountain winter bread wheat”.Conclusion. The identified 17 accessions resistant to Ptr are potential breeding sources of resistance. In the studied set of accessions, no significant relationship was found between the allelic state of the Tsn1 gene in the accession and its response to the infection with pathogen populations, including isolates with the ToxA gene.

Parental selection proposal strategy for recurrent selection in tropical wheat breeding

AbstractRecurrent selection is an effective breeding method for improving complex traits in wheat (Triticum aestivum L.) breeding. In this study, we propose a genitor selection strategy, employing a multi‐trait selection approach and genetic diversity analysis. To evaluate our proposed method, we conducted a lattice design trial during the winter seasons of 2020 and 2021 in Viçosa, MG, Brazil, comprising 87 lines and 13 commercial cultivars. It assessed various traits such as plant height, days to heading, wheat leaf rust, tan spot of wheat, a hundred grain mass, hectoliter weight, and grain yield, and the best linear unbiased predictor (BLUP) was obtained for each trait via restricted maximum likelihood. Next, a genotypic distance matrix, derived from principal component analysis using the BLUP values, was computed to perform hierarchical clustering via the unweighted pair group method with arithmetic mean. The selection of superior genotypes was made utilizing the multi‐trait genotype‐ideotype distance index, resulting in the identification of eight lines and two commercial cultivars as candidates. Furthermore, the genetic diversity analysis revealed distinct clusters among the selected genotypes. To assess the divergence of the chosen genitors, this study proposes a complementarity matrix using factor analysis. Our results indicate that this selection strategy effectively directed the identification of the best and divergent genitors. The complementarity matrix developed in this paper to evaluate the crossings proposal can also be used to evaluate combinations in any panel selected via a multi‐trait approach and can be easily applied and interpreted by breeders of various programs.

Association Mapping of Resistance to Tan Spot in the Global Durum Panel.

Tan spot, caused by the necrotrophic fungal pathogen Pyrenophora tritici-repentis (Ptr), is an important disease of durum and common wheat worldwide. Compared with common wheat, less is known about the genetics and molecular basis of tan spot resistance in durum wheat. We evaluated 510 durum lines from the Global Durum Wheat Panel (GDP) for sensitivity to the necrotrophic effectors (NEs) Ptr ToxA and Ptr ToxB and for reaction to Ptr isolates representing races 1 to 5. Overall, susceptible durum lines were most prevalent in South Asia, the Middle East, and North Africa. Genome-wide association analysis showed that the resistance locus Tsr7 was significantly associated with tan spot caused by races 2 and 3, but not races 1, 4, or 5. The NE sensitivity genes Tsc1 and Tsc2 were associated with susceptibility to Ptr ToxC- and Ptr ToxB-producing isolates, respectively, but Tsn1 was not associated with tan spot caused by Ptr ToxA-producing isolates, which further validates that the Tsn1-Ptr ToxA interaction does not play a significant role in tan spot development in durum. A unique locus on chromosome arm 2AS was associated with tan spot caused by race 4, a race once considered avirulent. A novel trait characterized by expanding chlorosis leading to increased disease severity caused by the Ptr ToxB-producing race 5 isolate DW5 was identified, and this trait was governed by a locus on chromosome 5B. We recommend that durum breeders select resistance alleles at the Tsr7, Tsc1, Tsc2, and the chromosome 2AS loci to obtain broad resistance to tan spot.

Evolution of the Genetic Structure of the Didymella tanaceti Population During Development of Succinate Dehydrogenase Inhibitor Resistance.

Emergence of pathogens with decreased sensitivity to succinate dehydrogenase inhibitor fungicides is a global agronomical issue. Analysis of Didymella tanaceti isolates (n = 173), which cause tan spot of pyrethrum (Tanacetum cinerariifolium), collected prior to (2004 to 2005) and after (2009, 2010, 2012, and 2014) the commercial implementation of boscalid in Tasmanian pyrethrum fields identified that insensitivity developed over time and has become widespread. To evaluate temporal change, isolates were characterized for frequency of mutations in the succinate dehydrogenase (Sdh) B, C, and D subunits associated with boscalid resistance, mating type, and SSR genotype. All isolates from 2004 and 2005 exhibited wild-type (WT) Sdh alleles. Seven known Sdh substitutions were identified in isolates collected from 2009 to 2014. In 2009, 60.7% had Sdh substitutions associated with boscalid resistance in D. tanaceti. The frequency of WT isolates decreased over time, with no WT isolates identified in 2014. The frequency of the SdhB-H277Y genotype increased from 10.7 to 77.8% between 2009 and 2014. Genotypic evidence suggested that a shift in the population structure occurred between 2005 and 2009, with decreases in gene diversity (uh; 0.51 to 0.34), genotypic evenness (E5; 0.96 to 0.67), genotypic diversity (G; 9.3 to 6.8), and allele frequencies. No evidence was obtained to support the rapid spread of Sdh genotypes by clonal expansion of the population. Thus, insensitivity to boscalid has developed and become widespread within a diverse population within 4 years of usage. These results suggest that D. tanaceti can disperse insensitivity through repeated frequent mutation, sexual recombination, or a combination of both.

Genome-wide association analysis of tan spot disease resistance in durum wheat accessions from Tunisia.

Background: Tunisia harbors a rich collection of unexploited durum wheat landraces (Triticum durum ssp. durum) that have been gradually replaced by elite cultivars since the 1970s. These landraces represent an important potential source for broadening the genetic background of elite durum wheat cultivars and for the introgression of novel genes for key traits, including disease resistance, into these cultivars. Methods: In this study, single nucleotide polymorphism (SNP) markers were used to investigate the genetic diversity and population structure of a core collection of 235 durum wheat accessions consisting mainly of landraces. The high phenotypic and genetic diversity of the fungal pathogen Pyrenophora tritici-repentis (cause of tan spot disease of wheat) in Tunisia allowed the assessment of the accessions for tan spot resistance at the adult plant stage under field conditions over three cropping seasons. A genome-wide association study (GWAS) was performed using a 90k SNP array. Results: Bayesian population structure analysis with 9191 polymorphic SNP markers classified the accessions into two groups, where groups 1 and 2 included 49.79% and 31.49% of the accessions, respectively, while the remaining 18.72% were admixtures. Principal coordinate analysis, the unweighted pair group method with arithmetic mean and the neighbor-joining method clustered the accessions into three to five groups. Analysis of molecular variance indicated that 76% of the genetic variation was among individuals and 23% was between individuals. Genome-wide association analyses identified 26 SNPs associated with tan spot resistance and explained between 8.1% to 20.2% of the phenotypic variation. The SNPs were located on chromosomes 1B (1 SNP), 2B (4 SNPs), 3A (2 SNPs), 3B (2 SNPs), 4A (2 SNPs), 4B (1 SNP), 5A (2 SNPs), 5B (4 SNPs), 6A (5 SNPs), 6B (2 SNPs), and 7B (1 SNP). Four markers, one on each of chromosomes 1B, and 5A, and two on 5B, coincided with previously reported SNPs for tan spot resistance, while the remaining SNPs were either novel markers or closely related to previously reported SNPs. Eight durum wheat accessions were identified as possible novel sources of tan spot resistance that could be introgressed into elite cultivars. Conclusion: The results highlighted the significance of chromosomes 2B, 5B, and 6A as genomic regions associated with tan spot resistance.

Resistance of spring bread wheat cultivars and lines to Septoria leaf blotch, tan spot, and spot blotch pathogens

Background. Leaf and stem diseases of cereal crops are among the most harmful in the agrocenoses of Tambov Province, significantly reducing grain yield and rapidly progressing in many regions of Russia. The aim of the study was to identify spring bread wheat lines and cultivars developed at the Middle-Russian Branch of the I.V. Michurin Federal Science Center that show resistance to leaf and stem diseases.Materials and methods. The target material was represented by 3 cultivars and 23 breeding lines of spring bread wheat. Disease resistance in seedlings was assessed in the laboratory, while for adult plants the process was carried out in the field in 2020–2022. The presence of the Tsn1 allele controlling susceptibility to the PtrToxA fungal toxin was detected using the Xfcp623 molecular marker.Results and conclusions. Accessions with high levels of resistance to Zymoseptoria tritici were identified: L-8252, L-82/60, L-8107, L-8078(23), L-43-9, L-43-1, L-4, Stb-8/15, Stb-7/15, and Stb-92. Accessions Stb-97, Stb-89, Stb-89(a), Stb-90, Stb-34, and Rl-6-22 were resistant to Parastagonospora nodorum; L-8134, L-8114, L-82/60, L-8107, Stb-10/15, Stb-9/15, Stb-8/15, Stb-7/15, Stb-97, Stb-89, Stb-89(a), Stb-90, Stb-34, and Rl-6-22 to P. pseudonodorum; L-8252, L-8107, L-43-9, L-43-1, L-4, Stb10/15, Stb-9/15, Stb-97, Stb-92, Stb-92(a), Stb-89, Stb-89(a), and Stb-34 to Pyrenophora tritici-repentis; and L-8114, L-82/60, L-43-9, L-43-1, L-4, Stb-90, Stb-34, and Rl-6-22 to Bipolaris sorokiniana. The cultivars and breeding lines showed group resistance to two, three or four pathogens. It was Lines L-8252, L-8134, L-82/60, L-8107, L-8078 (23), L-43-9, L-43-1, L-4, Stb-89, Stb-90, Stb-34, and L-33809-7-3 were observed to carry the recessive allele of the tsn1 gene.