Search

Tan 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. [ABSTRACT FROM AUTHOR]

The virulence of 57 Australian isolates of Pyrenophora tritici‐repentis (Ptr), a necrotrophic fungal pathogen responsible for the major wheat disease tan spot, was assessed through plant infection assays. Isolates collected from the northern, southern, and western wheat‐cropping regions of Australia were evaluated against 16 Australian bread wheat cultivars under controlled growth conditions. Following infection, the wheat panel displayed varying disease symptoms ranging from tiny necrotic specks to spreading chlorotic and necrotic lesions. Analysis of variance indicated that the wheat cultivar exhibited a greater effect on the disease response, explaining 62.7% of the variation, in comparison to the isolate (10.4%). The interaction between the cultivar and the isolate was statistically significant and was attributed to 9.8% of the total variation. All Ptr isolates examined were able to cause disease, but did not display a clear distinction in virulence on the wheat panel investigated, instead showing subtle differences in aggressiveness. Based on the disease responses, there was no obvious pattern between isolate aggressiveness and cropping region. Some cultivars, such as Hydra, exhibited an effective level of resistance in relation to the panel of isolates tested. All 57 Ptr isolates were found to possess the ToxA effector gene and lack the ToxB effector gene. The gene expression level of ToxA was up‐regulated at 3 days postinfection in both ToxA‐sensitive and ‐insensitive cultivars, independent of ToxA–Tsn1 recognition. [ABSTRACT FROM AUTHOR]

Assessment of quality and freshness of broodlac produced by the Indian lac insect Kerria lacca (Kerr) is an important parameter in its pricing. The present study provides an assessment of broodlac quality with 25, 50, 75 and 100% of lac encrustation harvested from summer (baisakhi), rainy (katki) on palas, winter (aghani) on ber, and summer season (jethwi) on kusum. The curve fitting model based on the rate of weight reduction can be used for prediction of freshness. Among the four lac crops, maximum rate of reduction was observed with summer kusmi (jethwi) and rangeeni (baisakhi) crops, and a good quality of broodlac was observed with katki crop on palas. Crawler emergence, stages of yellow spots and number of days for actual crawler emergence varied in different seasons. The present study differentiates the embryonic development into six stages with yellow spots through microscopic images. This reveals that the stage 1 coincides with earlier defined stage 2 and 3, and stage 2, 3, 4 and 5 are of stages 4, 5, 6 and 7 and 8, respectively. [ABSTRACT FROM AUTHOR]

This paper presents a smart system for the early detection of agricultural plant diseases in the vegetation period. The proposed smart system allows the detection of three types of wheat diseases, particularly yellow rust, powdery mildew, and Septoria at an early stage, and significantly improves the soil and ecology by locally spraying harmful chemicals just on sick plants. The proposed disease-detecting method is based on the structure of a convolutional neural network (CNN) using the Pycharm program based on the C ++ programming language. The basic structure of the smart system consists of Raspberry PI 4 MODULE, Raspberry Pi camera module v2, buzzer, HC-SR04 distance sensor, rotor driver, AC motor, power supply, relay microelectronics, and some digital devices.

Objectives: The assembly of fungal genomes using short-reads is challenged by long repetitive and low GC regions. However, long-read sequencing technologies, such as PacBio and Oxford Nanopore, are able to overcome many problematic regions, thereby providing an opportunity to improve fragmented genome assemblies derived from short reads only. Here, a necrotrophic fungal pathogen Pyrenophora tritici-repentis (Ptr) isolate 134 (Ptr134), which causes tan spot disease on wheat, was sequenced on a MinION using Oxford Nanopore Technologies (ONT), to improve on a previous Illumina short-read genome assembly and provide a more complete genome resource for pan-genomic analyses of Ptr. Results: The genome of Ptr134 sequenced on a MinION using ONT was assembled into 28 contiguous sequences with a total length of 40.79 Mb and GC content of 50.81%. The long-read assembly provided 6.79 Mb of new sequence and 2846 extra annotated protein coding genes as compared to the previous short-read assembly. This improved genome sequence represents near complete chromosomes, an important resource for large scale and pan genomic comparative analyses. [ABSTRACT FROM AUTHOR]

Metal homeostasis is integral to normal plant growth and development. During plant–pathogen interactions, the host and pathogen compete for the same nutrients, potentially impacting nutritional homeostasis. Our knowledge of outcome of the interaction in terms of metal homeostasis is still limited. Here, we employed the X-ray fluorescence microscopy (XFM) beamline at the Australian Synchrotron to visualize and analyse the fate of nutrients in wheat leaves infected with Pyrenophora tritici-repentis , a necrotrophic fungal pathogen. We sought to (i) evaluate the utility of XFM for sub-micron mapping of essential mineral nutrients and (ii) examine the spatiotemporal impact of a pathogen on nutrient distribution in leaves. XFM maps of K, Ca, Fe, Cu, Mn, and Zn revealed substantial hyperaccumulation within, and depletion around, the infected region relative to uninfected control samples. Fungal mycelia were visualized as thread-like structures in the Cu and Zn maps. The hyperaccumulation of Mn in the lesion and localized depletion in asymptomatic tissue surrounding the lesion was unexpected. Similarly, Ca accumulated at the periphery of the symptomatic region and as microaccumulations aligning with fungal mycelia. Collectively, our results highlight that XFM imaging provides the capability for high-resolution mapping of elements to probe nutrient distribution in hydrated diseased leaves in situ. [ABSTRACT FROM AUTHOR]

Tan spot (TS), caused by the fungus Pyrenophora tritici-repentis (Died) Drechs, is an important foliar disease of wheat and has become a threat to world wheat production since the 1970s. In this study a globally diverse pre-1940s collection of 247 wheat genotypes was evaluated against Ptr ToxA, P. tritici-repentis race 1, and stem rust to determine if; (i) acquisition of Ptr ToxA by the P. tritici-repentis from Stagonospora nodorum led to increased pathogen virulence or (ii) incorporation of TS susceptibility during development stem rust resistant cultivars led to an increase in TS epidemics globally. Most genotypes were susceptible to stem rust; however, a range of reactions to TS and Ptr ToxA were observed. Four combinations of disease-toxin reactions were observed among the genotypes; TS susceptible-Ptr ToxA sensitive, TS susceptible-Ptr ToxA insensitive, TS resistant-Ptr ToxA insensitive, and TS resistant-Ptr ToxA toxin sensitive. A weak correlation (r = 0.14 for bread wheat and −0.082 for durum) was observed between stem rust susceptibility and TS resistance. Even though there were no reported epidemics in the pre-1940s, TS sensitive genotypes were widely grown in that period, suggesting that Ptr ToxA may not be an important factor responsible for enhanced prevalence of TS.

Abstract Objectives The fungus Pyrenophora tritici-repentis is a major pathogen of wheat worldwide, causing the leaf spotting disease tan spot. To best inform approaches for plant genetic resistance, an understanding of the biology and pathogenicity mechanisms of this fungal pathogen is essential. Here, intracellular and extracellular proteins of P. tritici-repentis were extracted, and peptides analysed via high-resolution mass spectrometry. Our objective was to generate a useful proteomics resource for P. tritici-repentis. A survey of proteins secreted by the pathogen into culture filtrate is especially useful, as these are likely to come in direct contact with the wheat host and may play important roles in infection/pathogenicity. The peptide data presented herein, has also been used to successfully verify and refine in silico predicted P. tritici-repentis gene annotations, through the validation of alternative splicing and reading frame shifts. Data description The data sets presented consist of peptide spectra of the extracellular and intracellular proteomes of three P. tritici-repentis isolates. Peptide matches to translated transcripts of the North American reference isolate Pt-1C-BFP are also provided.

After nearly 40 years of DNA molecular marker development in plant breeding, the wheat research community has amassed an extensive collection of molecular markers which have been widely and successfully used for selection of agronomic, physiological and disease resistance traits in wheat breeding programs. Tan spot is a major fungal disease of wheat and a significant global economic challenge and is caused by the necrotrophic fungal pathogen Pyrenophora tritici-repentis (Ptr). Here, the potential for using a PCR-based marker (Ta1AS3422) present on the short arm of wheat chromosome 1A, was evaluated for effectiveness in distinguishing tan spot disease susceptibility. The marker was initially screened against 40 commercial Australian hexaploid wheat varieties, and those that amplified the marker had an overall lower disease score (2.8 ± 0.7 for seedlings and 2.4 ± 0.4 for plants at the tillering stage), compared to those lacking the marker which exhibited a higher disease score (3.6 ± 0.8 for both growth stages). The potential of Ta1AS3422 as a marker for the tan spot disease response was further assessed against a panel of 100 commercial Australian hexaploid wheat varieties. A significant association was observed between marker absence/presence and tan spot disease rating (Pearson’s chi-squared test, χ2 (6) = 20.53, p = 0.002), with absence of Ta1AS3422 associated with susceptibility. This simple and cost-effective PCR-based marker may be useful for varietal improvement against tan spot, although further work is required to validate its effectiveness.

Here, we evaluate the expression of the proteinaceous effectors ToxA and ToxB, produced by the necrotrophic fungal pathogen Pyrenophora tritici-repentis , which confer tan spot disease susceptibility on wheat. These necrotrophic effectors were expressed in two heterologous systems: Escherichia coli and Pichia pastoris. The E. coli SHuffle system was demonstrated to be superior to P. pastoris in generating high-levels of recombinant proteins that were soluble and stable. In addition, protein extracts from P. pastoris induced non-specific chlorosis on wheat, postulated to be caused by co-purified glucanases secreted by the host. Up to 79.6 μg/ml of ToxB was obtained using the SHuffle system in the absence of the native signal peptide, whilst the ToxA yield was considerably lower at 3.2 μg/ml. Results indicated that a histidine tag at the ToxA C-terminus interfered with effector functionality. Heterologously expressed ToxA and ToxB were tested on a panel of Australian cereals, including 122 varieties of bread wheat, 16 durum, 20 triticale and 5 barley varieties, as well as common plant model species including tobacco and Arabidopsis thaliana. A varying degree of effector sensitivities was observed, with a higher ToxB sensitivity and prevalence in the durum and triticale varieties. ToxB-induced chlorosis was also detected on barley. The heterologous expression of effectors that are easily scalable, will facilitate effector-assisted selection of varieties in wheat breeding programs as well as the investigation of P. tritici-repentis effectors in host and non-host interactions. [ABSTRACT FROM AUTHOR]

The incidence of wheat head infection by Pyrenophora tritici-repentis (Ptr), the etiological agent of tan spot disease, was evaluated during grain development in a glasshouse experiment. Heads artificially inoculated with a Ptr spore suspension developed widespread brown spots across the spikelets, and mycelia and conidophores were observed on glumes and awns. Seeds of heavily infected heads were darkened and shrivelled, but no red smudge symptoms were apparent. The recovery rate of Ptr isolates from the inoculated wheat heads was low, and colonies that were re-isolated displayed an irregular morphology with reddish mycelia when grown on agar plates. The presence of Ptr on inoculated wheat heads was assessed directly via PCR detection, and a limitation of Ptr hyphae to proliferate beyond the point of contact of spore inoculum on floret tissues was observed. The systemic transmission of Ptr from infected seeds was minimal; however, saprophytic growth of the pathogen occurred on the senescing leaves of wheat plants grown from inoculated seeds. Thus, even though Ptr seed infection is not as common as foliar infection, infected seeds are still a source of disease inoculum and screening for pathogen contamination is advisable.

This paper presents the results of pollen and spore concentration of yellow drops in the Lucknow environs during the summer of 2014. The yellow spots were procured from the surface of a number of leaves and other objects from three different localities of Lucknow District of Uttar Pradesh. The size and shapes of these spots vary, ranging from linear to circular. Pollen grains recovered in good frequencies chiefly belong to angiosperms, whereas some gymnosperm pollen was also observed in trace frequencies. Other microbiota include fern spores, fungal remains and insect body parts in lower values. The study broadly suggests that palynomorphs recovered from yellow droppings are not fully airborne; rather, they are the types that honey bees gather from crop fields to feed their young. Brassica campestris and Asteroideae are the dominant plant taxa recorded in yellow rain samples. On investigation, it was noticed that yellow drop falling occurred for a few minutes on limited days during the summer of 2014, when the atmosphere experienced optimal temperature conditions with relatively humid environs. The observation also confirms that the yellow spots are nothing but faecal droppings, as suggested by the bee faeces theory which proposed that the origin of yellow rain is a phenomenon of nature. The study, in addition to aiding in understanding yellow rain occurrence, could also be helpful in aerobiological research, especially in examining the allergenicity of various pollen grains/spores in the area of investigation, causing bronchial asthma, hay fever (allergic rhinitis/pollinosis), nasobronchial allergy and other respiratory disorders along with conjunctivitis, contact dermatitis, eczema, food allergies and other health ailments. A multivariate principal component analysis (PCA) was applied to quantified data obtained from pollen frequency analyses of different areas of Lucknow, which clearly revealed a significant group variation in vegetation type on the basis of dispersal and deposition of pollen in yellow spots. [ABSTRACT FROM AUTHOR]

The necrotrophic fungal pathogen Pyrenophora tritici‐repentis (Ptr) causes the major wheat disease tan spot, and produces multiple necrotrophic effectors that contribute to virulence. The proteinaceous effector ToxA induces necrosis in wheat genotypes possessing the Tsn1 gene, although the importance of the ToxA–Tsn1 interaction itself in varietal disease development has not been well studied. Here, 40 Australian spring wheat varieties were assessed for ToxA sensitivity and disease response to a race 1 wildtype Ptr isolate and ToxA‐deleted strain at both seedling and tillering growth stages. ToxA sensitivity was generally associated with disease susceptibility, but did not always predict spreading necrotic symptoms. Whilst the majority of Tsn1 varieties exhibited lower disease scores following toxa mutant infection, several exhibited no distinct differences between wildtype and toxa symptoms. This implies that ToxA is not the major determinant in tan spot disease development in some host backgrounds and indicates the presence of additional effectors. Unexpectedly, several tsn1 varieties exhibited a reduction in disease severity following toxa mutant inoculation, which may suggest an indirect role for ToxA in pathogen fitness. Additionally, increased chlorosis was observed following toxa mutant infection in three varieties, and further work is required to determine whether this is likely to be due to ToxA epistasis of ToxC symptoms. Taken together, these observations demonstrate that Ptr interacts with the host in a complex and intricate manner, leading to a variety of disease reactions that are dependent or independent of the ToxA–Tsn1 interaction. [ABSTRACT FROM AUTHOR]

We conducted experiments to test the influence of photo spacer PS on yellow spot and ripple. Results showed that the severity level of yellow spot and ripple can be lessened when main PS ratio reached more than 0.1%. Additionally, other PS parameters were further discussed. [ABSTRACT FROM AUTHOR]

Yellow spot (caused by Pyrenophora tritici-repentis) is a major foliar disease in wheat (Triticum aestivum) that has become more serious in recent years, possibly because of climate change. A major quantitative trait locus (QTL) located on the short arm of wheat chromosome 2B explaining 30-40% of the phenotypic variance has been identified as responsible for resistance to Australian yellow spot isolates, which reportedly produce mostly the ToxA effector. The closest marker linked to this QTL was a DArT marker not easy to use in large-scale selections, whereas the closest PCR-based marker available (2.7 cM) was too far away for reliably tagging the locus in wheat breeding. We therefore undertook studies to develop more closely linked and user-friendly markers for this major QTL. Forty-one new markers either synthesised from DArT markers or identified from the GrainGene database were assessed. From these, we developed a new PCR-based marker (Rfsts1), located 0.3 cM away from the major QTL. This is the first suitable marker for marker-assisted selection for yellow spot resistance in Australian wheat-breeding programs. [ABSTRACT FROM AUTHOR]

Objectives: The fungus Pyrenophora tritici-repentis is a major pathogen of wheat worldwide, causing the leaf spotting disease tan spot. To best inform approaches for plant genetic resistance, an understanding of the biology and pathogenicity mechanisms of this fungal pathogen is essential. Here, intracellular and extracellular proteins of P. triticirepentis were extracted, and peptides analysed via high-resolution mass spectrometry. Our objective was to generate a useful proteomics resource for P. tritici-repentis. A survey of proteins secreted by the pathogen into culture filtrate is especially useful, as these are likely to come in direct contact with the wheat host and may play important roles in infection/pathogenicity. The peptide data presented herein, has also been used to successfully verify and refine in silico predicted P. tritici-repentis gene annotations, through the validation of alternative splicing and reading frame shifts. Data description: The data sets presented consist of peptide spectra of the extracellular and intracellular proteomes of three P. tritici-repentis isolates. Peptide matches to translated transcripts of the North American reference isolate Pt- 1C-BFP are also provided. [ABSTRACT FROM AUTHOR]

• YS is an emerging physiological disorder negatively affecting lettuce production. • YS reduces photosynthesis and disrupts homeostasis of chemical elements. • YS is a heritable trait which manifestation is affected by environmental conditions. • YS-linked molecular markers can facilitate development of YS-resistant lines. Lettuce (Lactuca sativa L.) is an important leafy vegetable. An unknown malady that causes yellow spot (YS) blemishes on leaves has recently appeared in commercial fields in California, potentially reducing lettuce yield and/or quality. YS occurred on all morphological types of cultivated lettuce regardless of their color, with the highest (0.9) and lowest (0.09) rate in non-leaf (stem and oilseed) and leaf lettuce, respectively. The spots ranging in diameter from 0.5 to 3.1 mm (depending on genotype) were mostly observed on the adaxial leaf surface of mature or nearly mature plants. YS symptoms began as light-yellow circular spots that later became more intensely yellow and eventually turned necrotic. The YS affected area displayed decreased chlorophyll fluorescence and photosynthesis that were not caused by the effect of fungi, bacteria, viruses, insects, or foliar nematodes. Among 31 tested chemical elements, four macronutrients (P, Ca, Mg, and S) and eight microminerals (B, Cd, Cu, Li, Mn, Ni, Si, and Sn) had significantly changed concentration in the YS affected leaves. The trait exhibited a relatively high broad-sense inheritability (H2 = 47.9% ∼ 68.4%) in four experiments conducted at two locations in three years. The genome-wide association study (GWAS) involving 479 accessions revealed the effect of eight loci (qYS2.1, qYS3.1, qYS3.2, qYS4.1, qYS5.1, qYS5.2, qYS6.1 , and qYS7.1) defined by 10 significant SNP markers. A total of 162 genes were predicted in the identified chromosomal regions, with four oxidation-reduction (redox) catalyzers being potentially the most promising candidate genes involved in the regulation of this physiological disorder. [ABSTRACT FROM AUTHOR]

Yellow spots on leaves of white lace flower, Ammi majus, were found in Chiba Prefecture, Japan, in October 2006. The symptoms later developed into large brown spots. Brown lesions were also observed on the lower stem, and stem rot followed. A fungus was frequently isolated from the lesions, and the symptoms were reproduced after artificial inoculation. The causal fungus was identified as Pleospora herbarum based on morphology and molecular analysis. We named the new disease 'yellow spot' ('ouhan-byo' in Japanese). [ABSTRACT FROM AUTHOR]

The necrotrophic fungal pathogen Pyrenophora tritici-repentis causes tan spot, a major disease of wheat, throughout the world. The proteinaceous effector ToxA is responsible for foliar necrosis on ToxA-sensitive wheat genotypes. The single copy ToxA gene was deleted from a wild-type race 1 P. tritici-repentis isolate via homologous recombination of a knockout construct. Expression of the ToxA transcript was found to be absent in transformants ( toxa), as was ToxA protein production in fungal culture filtrates. Plant bioassays were conducted to test transformant pathogenicity. The toxa strains were unable to induce necrosis on ToxA-sensitive wheat genotypes. To our knowledge, this is the first demonstration of a targeted gene knockout in P. tritici-repentis. The ability to undertake gene deletions will facilitate the characterization of other pathogenicity effectors of this economically significant necrotroph. [ABSTRACT FROM AUTHOR]

Genetic disease resistance is widely assumed, and occasionally proven, to cause host yield or fitness penalties due to inappropriate activation of defence response mechanisms or diversion of resources to surplus preformed defences. The study of resistance gene trade-offs has so far been restricted to biotrophic pathogens. In some Pleosporales necrotrophic interactions, quantitative resistance is positively associated with insensitivity to effectors. Host lines that differ in sensitivity can easily be identified amongst current cultivars and advanced breeding lines. Large wheat cultivar trials were used to test whether lines sensitive or insensitive to three necrotrophic effectors from Pyrenophora tritici-repentis and Parastagonospora nodorum differed in yield when subjected to natural disease and stress pressures in the West Australian wheat belt. There was no significant yield penalty associated with insensitivity to the fungal effectors ToxA, SnTox1 and SnTox3. Some yield gains were associated with insensitivity and some of these gains could be attributed to increased disease resistance. It is concluded that insensitivity to these effectors does not render such plants more vulnerable to any relevant biotic or abiotic stress present in these trials. These results suggest that the elimination of sensitivity alleles for necrotrophic effectors is a safe and facile strategy for improving disease resistance whilst maintaining or improving other desirable traits. [ABSTRACT FROM AUTHOR]

Knowledge of genetic variation in a pathogen population contributes to breeding for disease resistance. The fungus Pyrenophora tritici-repentis, cause of tan spot of wheat, is an important foliar pathogen worldwide. Currently, eight races have been identified in the fungal population prevalent on wheat and alternative hosts. Races 1 through 6 have been observed in North America. However, the fungal population from South America has not been characterized as to race. In this study, 48 single-spore isolates of P. tritici-repentis, recovered from wheat, were obtained from Argentina (10), Brazil (23), and Uruguay (15). Isolates were tested by inoculating individually on 2-leaf stage seedlings of the wheat differentials Glenlea, Katepwa, ND495, 6B365, M-3, and Salamouni in the greenhouse. They were grouped into different races based on necrosis and chlorosis induction on the differentials. Isolates from Argentina were grouped into races 1 and 7; from Brazil into races 1 and 8; and, from Uruguay into races 1 and 2. Results indicate that P. tritici-repentis has a diverse population on wheat in South America. More isolates are under investigation to obtain a comprehensive virulence pattern of the pathogen population in South America. Wheat lines should be screened against all known races to achieve durable resistance in a cultivar release program. The P. tritici-repentis race structure on wheat in Europe needs to be determined, as the pathogen has become a concern for wheat breeders and pathologists.

This work was done to demonstrate the opportunities provided by application of meta-analysis in plant pathology. It was a case study used to determine the effectiveness of foliar fungicides in minimising yield loss from a complex of yellow spot ( Pyrenophora tritici- repentis) and septoria nodorum blotch ( Stagonospora nodorum, teleomorph: Phaeosphaeria nodorum) (YS-SNB disease complex) on wheat in the northern grain-belt of Western Australia. Forty-seven datasets of experimental results from 14 growing seasons, using 18 varieties sprayed one to three times, predominantly with tebuconazole or propiconazole fungicides, were analysed. Across the datasets, the wheat yield gain from fungicide application was 297 kg ha with a 95 % confidence interval of 11.6 kg ha. Significant yield gains resulted from single or multiple applications of fungicides. Both propiconazole and tebuconazole, increased yield of wheat affected by the YS-SNB disease complex, with yield gain from propiconazole being greater than that from tebuconazole. Yield response varied significantly among crop growing seasons. Meta-analysis was able to aggregate a large number of experimental results and answer important questions related to the variables that influenced those results; in this case the effectiveness of fungicides in minimising yield loss from the YS-SNB disease complex on wheat. It also identified areas where further research needs to be done. It is concluded that meta-analysis has the potential to contribute to similar analyses in other crop disease systems. [ABSTRACT FROM AUTHOR]

Tan spot, a major foliar disease of wheat ( Triticum aestivum L.), is caused by an ascomycete Pyrenophora tritici-repentis. Both culture filtrates and conidiospore inocula induce disease symptoms in susceptible wheat genotypes. The objectives of this study were to determine and map the genetic control of resistance to spore inocula and culture filtrates of P. tritici-repentis races 2 and 5. The F1 and F2 generations and an F2:6 recombinant inbred lines (RIL) population were developed from a cross between the resistant ND 735 and the susceptible Steele-ND. Disease assessments of the segregating generations were done at the seedling stage using culture filtrates and spore inocula under controlled environmental conditions. Genetic and mapping analyses of the F1 and F2 generations and the RIL by both methods indicated that the same single recessive gene, Tsr1, located on chromosome 5BL, controlled resistance and insensitivity to necrosis induced by race 2. A second recessive gene, designated Tsr6, located on chromosome 2BS, conferred resistance/insensitivity to chlorosis induced by spore inocula or culture filtrates of race 5. Diversity Arrays Technology markers wPt-3049 (2.9 cM) and wPt-0289 (4.6 cM) were closely linked to Tsr1 and Tsr6, respectively. The results further indicated that culture filtrates can be used as surrogates for spore inoculation. Tsr1 and Tsr6 can be selected by marker-assisted selection in breeding for resistance to tan spot. [ABSTRACT FROM AUTHOR]

Abstract: Tan spot, caused by Pyrenophora tritici-repentis (Died.) Drechs., is an important constraint to wheat (Triticum aestivum L.) yield in many countries. Since the inheritance of field resistance to tan spot is poorly understood, this study was conducted to determine the genetic control of resistance in the field. Resistance was measured as disease severity caused by P. tritici-repentis race 1 in four crosses involving five wheat parents: parent 1 (P1)=catbird; parent 2 (P2)=Milan/Shanghai-7; parent 3 (P3)=Alondra/Coc//Ures; parent 4 (P4)=Bcb//Dundee/Gul/3/Gul); parent 5 (P5)=ND/VG9144//Kal/BB/3/Yaco/4/Chil. P1, P2 and P3 were resistant and P4 was moderately resistant, whereas P5 was susceptible to tan spot. The F2-derived F3 families and the parents were field evaluated at El Batán, Mexico, in 1996. When all the plants within a F3 family expressed low levels of disease severity similar to that of the resistant parent it was classified resistant (R), otherwise the progeny was classified as susceptible (S). The progeny of the three crosses of the susceptible parent with the resistant and moderately resistant parents P2, P3, and P4 segregated as 3R:13S whereas the progeny in the cross with P1 showed a segregation ratio of 1R:15S. This suggests that each resistant parent possessed two genes conditioning resistance to tan spot severity caused by P. tritici-repentis race 1. Information on the inheritance of resistance measured as disease severity on adult plants under field conditions is of practical importance for wheat breeding programs seeking improvement in tan spot resistance. [Copyright &y& Elsevier]

The incidence of wheat head infection by Pyrenophora tritici-repentis (Ptr), the etiological agent of tan spot disease, was evaluated during grain development in a glasshouse experiment. Heads artificially inoculated with a Ptr spore suspension developed widespread brown spots across the spikelets, and mycelia and conidophores were observed on glumes and awns. Seeds of heavily infected heads were darkened and shrivelled, but no red smudge symptoms were apparent. The recovery rate of Ptr isolates from the inoculated wheat heads was low, and colonies that were re-isolated displayed an irregular morphology with reddish mycelia when grown on agar plates. The presence of Ptr on inoculated wheat heads was assessed directly via PCR detection, and a limitation of Ptr hyphae to proliferate beyond the point of contact of spore inoculum on floret tissues was observed. The systemic transmission of Ptr from infected seeds was minimal; however, saprophytic growth of the pathogen occurred on the senescing leaves of wheat plants grown from inoculated seeds. Thus, even though Ptr seed infection is not as common as foliar infection, infected seeds are still a source of disease inoculum and screening for pathogen contamination is advisable. [ABSTRACT FROM AUTHOR]