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Monosporascus cannonballus and M. eutypoides are the causative agents of melons' root rot and vine decline, with little knowledge about their mechanisms of infection. M. cannonballus secretome was isolated and subdivided into two fractions based on molecular weight (smaller and larger than 10 kDa), and further separated via high voltage paper electrophoresis and SDS-PAGE, respectively. Large cell-free filtrates of the fungus were found to contain biologically active proteins that were further characterized via mass spectrometry and revealed to be α-1,2-mannosidase and serine protease. Meanwhile, biochemical analyses of low molecular weight compounds were suggestive to be similar to marasmines. Both fractions were capable of inducing phytotoxicity, once infiltrated into the melon leaves. This is the first report of phytotoxic compounds isolated from M. cannonballus contributing to disease induction in melon plants. [ABSTRACT FROM AUTHOR]

Pyrenophora tritici-repentis (Ptr) is a destructive fungal pathogen of wheat worldwide. In addition to wheat, Ptr has been isolated from various other hosts in the family Poaceae, yet the nature of its interaction with those hosts is unknown. The Ptr-barley relationship was explored and the existence of a specific interaction between Ptr and barley is described for the first time; symptom development on several barley genotypes was evaluated in bioassays and by toxin infiltration into barley leaves. Ptr ToxB-producing isolates of the fungus were able to cause significant damage when inoculated onto certain barley genotypes, and Ptr ToxB was able to induce chlorosis in a highly selective manner when infiltrated into those same genotypes. Ptr-barley specificity is subtle and can break with slight changes in temperature after infection. To understand the infection process in barley, a cytological analysis and in planta fungal biomass estimation using quantitative PCR were performed. The fungus penetrates through the host epidermal cells and advances to colonize the mesophyll layer intercellularly, with the infection process on barley closely resembling that on wheat. Here, evidence is provided for a specific interaction between barley and Ptr, expanding understanding of Ptr host specificity and breaking the assumption that the highest level of specificity seen with Ptr is restricted to particular genotypes of the wheat host. [ABSTRACT FROM AUTHOR]

The population genetic structure of plant pathogenic fungus Pyrenophora tritici-repentis was examined using microsatellite (SSR) markers. According to the geographical origin of the pathogen populations, they were designated as North Caucasian (S, 33 isolates), northwest (Nw, 39), and Omsk (Om, 43). The populations were analyzed at the nine most polymorphic SSR loci, at which 75 alleles were identified. To characterize the genetic variation within and between populations, the AMOVA algorithm as implemented in the Arlequin v. 3.5 software program was used. The number of alleles per locus ranged from 5 to 12 and their sizes varied within the range from 180 to 400 bp. The mean gene diversity at SSR loci was high for all populations ( H = 0.58-0.75). The populations were considerably different in the frequencies of individual alleles of the SSR loci. Most isolates in the populations were represented by unique haplotypes. The within-population variation of the isolates at molecular markers was 86.4%; among the populations, 13.6%. Substantial interpopulation differences were found between the Om and S ( F = 0.16) and between the Om and Nw ( F = 0.20) populations, whereas between the S and Nw populations, these differences were small ( F = 0.05). Thus, it was demonstrated that the population of P. tritici-repentis from Omsk oblast had the independent status of the geographical population; northwest and North Caucasian populations differed in the allelic diversity of SSR loci, and despite the low F value (0.05), they also belonged to independent geographical populations. [ABSTRACT FROM AUTHOR]

Generalist plant pathogens may have wide host ranges, but many exhibit varying degrees of host specialization, with multiple pathogen races that have narrower host ranges. These races are often genetically distinct, with each race causing highest disease incidence on its host of origin. We examined host specialization in the seed pathogen Pyrenophora semeniperda by reciprocally inoculating pathogen strains from Bromus tectorum and from four other winter annual grass weeds (Bromus diandrus, Bromus rubens, Bromus arvensis and Taeniatherum caput-medusae) onto dormant seeds of B. tectorum and each alternate host. We found that host species varied in resistance and pathogen strains varied in aggressiveness, but there was no evidence for host specialization. Most variation in aggressiveness was among strains within populations and was expressed similarly on both hosts, resulting in a positive correlation between strain-level disease incidence on B. tectorum and on the alternate host. In spite of this lack of host specialization, we detected weak but significant population genetic structure as a function of host species using two neutral marker systems that yielded similar results. This genetic structure is most likely due to founder effects, as the pathogen is known to be dispersed with host seeds. All host species were highly susceptible to their own pathogen races. Tolerance to infection (i.e., the ability to germinate even when infected and thereby avoid seed mortality) increased as a function of seed germination rate, which in turn increased as dormancy was lost. Pyrenophora semeniperda apparently does not require host specialization to fully exploit these winter annual grass species, which share many life history features that make them ideal hosts for this pathogen. [ABSTRACT FROM AUTHOR]

Pyrenophora teres is the causal agent of net blotch fungus disease on barley, one of the most common, destructive foliar diseases in barley pathology. Abiotic factors play an important role for fungal development. Under laboratory conditions it was monitored the abiotic factors influence (temperature, light and culture media) on the Pyrenophora teres fungi growth and sporulation. The pathogen have been isolated from barley leaves of Dana variety and incubated at 22°C. Actual research monitored the biological thresholds on the growth and sporulation of Pyrenophora teres fungus. Regarding the temperature influence on the colonies development, the observations revealed that the pathogen growth begins at 6°C. The optimal pathogen development threshold is between 20 to 26°C temperatures, the fungus developing colonies measuring 90 mm after 9 days observations. Over 28°C temperature, the growth rate of the fungal colonies decreased, and at 34°C the fungus ceased sporulation. The light influence on the Pyrenophora teres fungi development showed that the colonies have been well developing under continuous light conditions, as well under 16/8 alternating light conditions, the colonies' diameter measuring 85 mm after 9 days observations. Under the continuous lack of light conditions (dark), the colony developed slowly, reaching a diameter of 65 mm after 15 days incubation. Under continuous light conditions, Pyrenophora teres had the fastest development rate, after 3 days of incubation the colony diameter reached 41 mm and respectively 87 mm, after 9 days of observations. Pyrenophora teres fungus had the optimal growth & development on the natural type culture media compared with artificial ones. [ABSTRACT FROM AUTHOR]

Background: Pyrenophora tritici-repentis is a phytopathogenic fungus which causes tan spot on wheat. Some races of P. tritici-repentis produce host-specific toxins which present symptoms of chlorosis or necrosis on susceptible wheat cultivars. One such toxin is Ptr ToxA, which enters mesophyll cells through a putative toxin-receptor and localizes with chloroplasts, ultimately causing damage and necrosis on leaves. These symptoms can occur even in the absence of the pathogen. Insensitive cultivars lack the receptor and Ptr ToxA cannot enter cells. The molecular mechanisms surrounding this plant-pathogen interaction are still largely unknown, although some details have begun to emerge. Results: Using 2-D electrophoresis, fifteen protein changes were identified reproducibly in the leaf proteomes of a sensitive and an insensitive cultivar over three days after inoculation of purified Ptr ToxA. Functional analysis of the proteins indicated that senescence signals may be induced in the sensitive cultivar. In the insensitive cultivar proteins involved in some features of senescence inhibition were seen. Complementary responses at the biochemical level may be actively promoting a localized senescence-like response in sensitive wheat cultivars whilst actively inhibiting this response in insensitive cultivars. Conclusion: This is the first report of a biochemical response in an insensitive cultivar in this plant-pathogen interaction. Findings support the involvement of ethylene, and the activation of complementary pathways in sensitive versus insensitive wheat cultivars responding to Ptr ToxA. The nature of the system permits using purified toxin to mimic disease, which eliminates the pathogen proteome and ensures a synchronous response in inoculated leaves. [ABSTRACT FROM AUTHOR]

Generalist pathogens can exhibit differential success on different hosts, resulting in complex host range patterns. Several factors operate to reduce realized host range relative to potential host range, particularly under field conditions. We explored factors influencing host range of the naturally occurring generalist ascomycete grass seed pathogen Pyrenophora semeniperda. We measured potential host range in laboratory experiments at high inoculum loads with 26 grass species, including the primary host Bromus tectorum, and developed models to predict susceptibility and tolerance based on host traits, including germination speed, seed hardness, seed size, and phylogenetic relations. We also examined pathogen and host density effects on infection and mortality. All species tested were at least somewhat susceptible to the pathogen at high inoculum loads, but both infection and mortality varied widely. Species more closely related to the original host ( B. tectorum) were more susceptible to infection, whereas species with slower germination were less tolerant and therefore more likely to suffer mortality. Infection and mortality were sharply reduced as inoculum load was reduced. Intermediate loads had major negative impacts on dormant B. tectorum seeds but generally minimal effects on native species. In addition, field seed bank studies determined that P. semeniperda rarely exploits native grass species as hosts. This marked reduction in realized host range relative to potential host range indicates that laboratory host range studies are potentially a poor predictor of either the current or possible future realized host range for wildland plant pathogens. [ABSTRACT FROM AUTHOR]

A cDNA library was created on the basis of transcripts that were generated during the process of infection of wheat and barley with Pyrenophora tritici-repentis or P. teres. Due to the time course of infection assays, the leaves were collected at various intervals after inoculation until 100 h after inoculation. We compared the temporal development of the two pathogens, as well as the effect of varieties of the same crop species, and differences among isolates of a single pathogen. The appressoria and vesicular structures developed more rapidly in barley varieties inoculated by P. teres than in wheat varieties inoculated by P. tritici-repentis. The lower level of susceptibility of the wheat variety Globus and the barley variety Heris to P. tritici-repentis and P. teres, respectively, was apparent from 12 h after infection. Information on changes in expression profiles during pathogenesis and on the clones that could be functionally assigned to the known gene sequences is presented. Out of the 360 transcript derived fragments (TDFs) produced in the barley-P. teres pathosystem in our trials, 62% were specific to the plant-pathogen interaction. In the wheat-P. tritici-repentis pathosystem 291 TDFs occurred, 63% were specific to the plant-pathogen interaction. [ABSTRACT FROM AUTHOR]

SUMMARY The fungus Pyrenophora tritici-repentis causes tan spot, a wheat leaf disease of worldwide importance. The pathogen produces three host-selective toxins, including Ptr ToxB, which causes chlorophyll degradation and foliar chlorosis on toxin-sensitive wheat genotypes. The ToxB gene, which codes for Ptr ToxB, was silenced in a wild-type race 5 isolate of the fungus thorough a sense- and antisense-mediated silencing mechanism. Toxin production by the silenced strains was evaluated in culture filtrates of the fungus via Western blotting analysis, and plant bioassays were conducted to test the virulence of the transformants in planta. The chlorosis-inducing ability of the silenced strains was correlated with the quantity of Ptr ToxB, and transformants in which toxin production was strongly decreased also caused very little disease on toxin-sensitive wheat genotypes. Cytological analysis of the infection process revealed that, in addition to a reduced capacity to induce chlorosis, the silenced strains with the greatest decrease in the levels of Ptr ToxB produced significantly fewer appressoria than the wild-type isolate, 12 and 24 h after inoculation onto wheat leaves. The results provide strong support for the suggestion that the amount of Ptr ToxB protein produced by fungal isolates plays a significant role in the quantitative variation in the virulence of P. tritici-repentis. [ABSTRACT FROM AUTHOR]

Tan spot, caused by Pyrenophora tritici-repentis, is an important disease of wheat worldwide. To manage tan spot, quinone outside inhibitor (QoI) fungicides such as azoxystrobin and pyraclostrobin have been applied in many countries. QoI fungicides target the cytochrome b (cyt b) site in complex III of mitochondria and, thus, pose a serious risk for resistance development. The resistance mechanism to QoI fungicides is mainly due to point mutations in the cyt b gene. The objective of this study was to develop a molecular detection method for the four currently known mutations responsible for shifts in sensitivity toward QoI fungicides in P. tritici-repentis. Twelve specific primers were designed based on sequences from the National Center for Biotechnology Information accessions AAXI01000704 and DQ919068 and used to generate a fragment of the cyt b gene which possesses four known single-nucleotide polymorphisms (SNPs). These mutant clones served as positive controls because QoI-insensitive and -reduced-sensitive isolates of P. tritici-repentis have not yet been reported in the United States. The partial cyt b gene clones were sequenced to identify the SNPs at sites G143A and F129L. Genomic DNA of the mutated partial cyt b gene clones and the European QoI-insensitive and -reduced-sensitive isolates of P. tritici-repentis possessing G143A (GCT) and F129L (TTA, TTG, and CTC) mutations were amplified by polymerase chain reaction (PCR) using two specific primer pairs and were further digested with three specific restriction enzymes (BsaJI, Fnu4HI, and MnlI). The results of the digested PCR product from genomic DNA of known QoI-insensitive and -reduced-sensitive isolates of P. tritici-repentis had DNA bands consistent with the mutation GCT at G143A and the mutations TTA, TTG, and CTC at F129L. The amplified region at the F129 site also had 99% sequence similarity with P. teres, the net blotch pathogen of barley. To validate mutations, we further tested two isolates of P. teres known to have reduced sensitivity to QoI fungicides possessing the mutations TTA and CTC at F129L. After PCR amplification and restriction digestion, DNA bands identical to those observed for the partial cyt b mutant clones were detected. These results suggest that this newly developed two-step molecular detection method is rapid, robust, and specific to monitor QoI-insensitive and -reduced-sensitive isolates of P. tritici-repentis. [ABSTRACT FROM AUTHOR]

Tan spot, caused by Pyrenophora tritici- repentis, is a major foliar disease of wheat worldwide. Host plant resistance is the best strategy to manage this disease. Traditionally, bi-parental mapping populations have been used to identify and map quantitative trait loci (QTL) affecting tan spot resistance in wheat. The association mapping (AM) could be an alternative approach to identify QTL based on linkage disequilibrium (LD) within a diverse germplasm set. In this study, we assessed resistance to P. tritici- repentis races 1 and 5 in 567 spring wheat landraces from the USDA-ARS National Small Grains Collection (NSGC). Using 832 diversity array technology (DArT) markers, QTL for resistance to P. tritici- repentis races 1 and 5 were identified. A linear model with principal components suggests that at least seven and three DArT markers were significantly associated with resistance to P. tritici- repentis races 1 and 5, respectively. The DArT markers associated with resistance to race 1 were detected on chromosomes 1D, 2A, 2B, 2D, 4A, 5B, and 7D and explained 1.3-3.1% of the phenotypic variance, while markers associated with resistance to race 5 were distributed on 2D, 6A and 7D, and explained 2.2-5.9% of the phenotypic variance. Some of the genomic regions identified in this study correspond to previously identified loci responsible for resistance to P. tritici- repentis, offering validation for our AM approach. Other regions identified were novel and could possess genes useful for resistance breeding. Some DArT markers associated with resistance to race 1 also were localized in the same regions of wheat chromosomes where QTL for resistance to yellow rust, leaf rust and powdery mildew, have been mapped previously. This study demonstrates that AM can be a useful approach to identify and map novel genomic regions involved in resistance to P. tritici- repentis. [ABSTRACT FROM AUTHOR]

Tan spot, caused by Pyrenophora tritici-repentis, is a foliar disease of wheat, responsible for high economic losses in several wheat growing areas in the world. There are eight known races of P. tritici-repentis based on ability to induce necrosis and/or chlorosis on a set of differential cultivars. Fifty five isolates of P. tritici-repentis originating from diverse wheat growing regions in Algeria were studied to determine which races are present and to identify new races. Races 1, 4, 5, 6, 7 and 8 were found and a new virulence pattern was identified. Isolates with this pattern induced necrosis in durum wheat but failed to induce any disease in the common wheat genotypes in the differential set. [ABSTRACT FROM AUTHOR]

Knowledge of the virulence of a pathogen population and recognition of the risks of changes in the virulence spectrum are essential in breeding crops for disease resistance. Sexual recombination in a pathogen increases the level of genotypic diversity and can influence the virulence spectrum. This study aimed to determine how sexual recombination can change virulence of the barley pathogen Pyrenophora teres and whether the barley cultivation system, no-tillage or normal tillage, influences P. teres virulence. The inheritance of avirulence/virulence in P. teres following sexual reproduction was studied in three artificially created pathogen populations. The first was a product of crossing two net forms of the pathogen, and the second and the third were products of crossing net and spot forms. None of the progeny generated resembled the parents exactly. The average similarity of the progeny isolates of the net by net cross with the parental type, based on avirulence/virulence tests, was 92%. That for net and spot form progenies was 58% in comparison with the net form parents and 73% with the spot form parents. The virulence reactions of the progeny isolates did not correlate with morphological traits of the isolates: growth rate on agar, spore production, spore width, spore length and numbers of septa per conidium. To study the effect of the barley cultivation method on P. teres virulence, 313 single-spore cultures were obtained from barley fields. Two hundred and seventy-six of the isolates represented the spot form and 37 represented the net form of P. teres. No association was established between the tillage method and virulence for either the net form or the spot form isolates. [ABSTRACT FROM AUTHOR]

The fungus Pyrenophora tritici-repentis can infect wheat kernels, causing red smudge, and has been shown to produce the anthraquinone mycotoxins emodin, catenarin, and islandicin. The growth of 8 fungal isolates from diverse regions was evaluated on various culture media and was found to be generally slowest on the semisynthetic Fries medium. The choice of carbon source had a significant effect on mycotoxin production, as assessed by high-performance liquid chromatography. The highest emodin concentration (194.18 ± 16.26 µg/g medium) was observed for isolate Alg 3-24 on Fries medium supplemented with fructose, while the highest catenarin concentration (302.54 ±13.92 µg/g medium) was observed for TS93-71B on Fries medium supplemented with starch. Islandicin was not produced by any isolate under the conditions tested. Evaluation of the dynamics of mycotoxin production by isolate 331-2 on V8-potato dextrose agar medium revealed a rapid accumulation of emodin and catenarin during the first week of incubation, followed by a large decline by 14 days. Differences in the growth of and mycotoxin production by isolates of P. tritici-repentis likely resulted from the differential composition of the media and (or) intraspecies variability. Accordingly, the optimization of growth medium should be considered when evaluating the potential of specific isolates for mycotoxin production. Le champignon Pyrenophora tritici-repentis infecte les grains de blé, causant la maladie de la tache auréolée, et produit de l'émodine, de la caténarine, et de l'islandicine, des mycotoxines anthraquinones. La croissance de 8 isolats fongiques provenant de diverses régions a été évaluée dans différents milieux de culture, et a été trouvée généralement plus lente dans le milieu semi-synthétique Fries. Le choix de la source de carbone avait un effet significatif sur la production de mycotoxines, tel qu'évalué en chromatographie liquide à haute performance. La concentration la plus élevée d'émodine (194,18± 16,26 µg/g de milieu) a été observée chez l'isolat Alg 3-24 dans le milieu Fries supplémenté en fructose, alors que la concentration la plus élevée de caténarine (302,54 ± 13,92 µg/g de milieu) a été observée chez TS93-71B dans le milieu Fries supplémenté en amidon. L'islandicine n'était produite par aucun isolat dans les conditions testées. L'évaluation de la dynamique de production des mycotoxines par l'isolat 331-- dans une gélose V8-pomme de terre-dextrose a révélé une accumulation rapide d'émodine et de caténarine au cours de la première semaine d'incubation, suivie d'une diminution importante après 14 jours. Les différences dans la croissance et la production de mycotoxines par les isolats de P. tritici-repentis résultent vraisemblablement de la composition différentielle du milieu et (ou) de la variabilité intra-espèce. Ainsi, l'optimisation du milieu de culture devrait être prise en compte dans l'évaluation du potentiel de production de mycotoxines par des isolats spécifiques. [ABSTRACT FROM AUTHOR]

Pyrenophora tritici-repentis, the causal agent of tan spot on wheat, is a homothallic loculoascomycete with a complex race structure. The objectives of this study were to confirm the homothallic nature of the pathogen, characterize mating type diversity and toxin production genes in a global collection of strains, and analyze how these traits are associated between each other and with existing races. The pseudothecia production capacity, race identification, mating type locus (MAT), internal transcribed spacer, and glyceraldehyde-3-phosphate dehydrogenase regions were analyzed in a selection of 88 strains originating from Europe, North and South America, North Africa, and Central and South Asia. Some (60%) strains produced pseudothecia containing ascospores, independent of their origin. Race identification obtained using the multiplex polymerase chain reaction targeting host-selective toxin (HST) genes was consistent, overall, with the results based on the inoculation of a set of differential wheat cultivars and confirmed the predominance of race 1/2 strains (≈83%). However, discrepancies in race identification, differences from the reference tester strains, and atypical ToxA profiles suggest the presence of new races and HSTs. The MAT1-1 and MAT1-2 coding regions are consecutively arranged in a single individual, suggesting putative heterothallic origin of P. tritici-repentis. Upstream from the MAT is an open reading frame of unknown function (ORFI) containing a MAT-specific degenerate carboxy-terminus. The phylogenetic analysis of the MAT locus reveals two distinct groups, unlinked to geographical origin or ToxA profile. Group 1, the best-represented group, is associated with typical tan spot lesions caused by races 1, 2, 3, and 5 on wheat. It is more homogenous than group II encompassing race 4 strains, as well as isolates associated primarily with small spot lesions on wheat leaves or other hosts. Group II could contain several distinct taxa. [ABSTRACT FROM AUTHOR]

A 21-year-old Appaloosa mare was presented with a pigmented cutaneous mass at the base of the right side of the neck. The diagnosis of phaeohyphomycosis due to pigmented fungi, known as Pyrenophora phaeocomes and Drechslera nobleae, was made based on a histopathology report followed by polymerase chain reaction (PCR) and 18S rRNA gene sequencing. The mass was surgically excised with clean margins, which is usually curative. Une jument Appaloosa âgée de 21 ans a été présentée avec une masse cutanée pigmentée à la base du côté droit du cou. Le diagnostic de phoeohyphomycose causée par des champignons pigmentés, connus sous le nom de Pyrenophora phaeocomes et de Drechslera nobleae, a été posé en se fondant sur un rapport d'histopathologie suivi d'une amplification en chaîne par la polymérase et d'un séquençage du gène 18S rRNA. La masse a été excisée chirurgicalement avec des bords nets, ce qui se traduit habituellement par la guérison. [ABSTRACT FROM AUTHOR]

The fungus Pyrenophora tritici- repentis (Died.) causes tan spot, an important leaf disease of wheat worldwide. Isolates of this pathogen have been collected and characterized into eight races on the basis of their ability to produce three different host-selective toxins. The karyotype of 47 isolates was determined by pulsed field gel electrophoresis. The collection originated from different parts of the world and included genotypes from all races. A single isolate was characterized for each of races 3, 4 and 6, whereas fourteen, five, nine, five and eleven isolates were karyotyped for races 1, 2, 5, 7 and 8, respectively. The survey showed that the chromosome number of P. tritici-repentis was highly variable, with some isolates having as few as eight chromosomes, but others having 11 or more. Similarly, the genome size ranged from 25.5 to 48.0 Mb, and individual chromosome sizes ranged from 1.3 to more than 5.7 Mb. Considerable variation was observed in karyotype patterns among the P. tritici-repentis isolates tested. A total of 29 different karyotypes was identified among the 47 isolates. These chromosome level variations were as variable for isolates within a race as for isolates across races. Southern blot analysis of the 47 isolates with ToxA and ToxB probes revealed that the toxin genes were always located on different chromosomes. Furthermore, with six chromosome-specific single-copy probes, the ToxA-carrying chromosome was shown to be homologous among the Ptr ToxA-producing isolates, with a related chromosome in the non-ToxA-producing isolates, suggesting that the chromosome on which ToxA generally resides is of an essential nature. Interestingly, a molecular rearrangement involving a translocation of ToxA to a different chromosome was identified in one isolate. [ABSTRACT FROM AUTHOR]

The article discusses a study which examined the natural incidence of disease caused by pathogen Pyrenophora (P.) semeniperda on undispersed host seeds of grass Bromus tectorum. The researchers found that at least 90% of undispersed seeds exhibiting the disease were infected after maturity by conidia borne. It concludes that studies on the life history of P. semeniperda and its genetic structure should further clarify the role of seed-assisted dispersal in the ecology of this pathogen.

Field experiments were carried out in 1982—83 and 1983—84 in Northern and Central Italy (3 locations) in order to investigate the effect of different levels of seed infection of Pyrenophora graminea on disease incidence and yield losses in 'Perga' winter barley. Six levels of natural seed infection, assessed by the deep-freezing blotter method have been compared in 8 row-plots, 7.5 m long, arranged in randomized blocks with 4 replications. The percentage of infected plants and tillers has been recorded in all locations and the yield in two of them. A highly significant correlation was found between seed infection, plant infection, tiller infection and yield reduction. Major ratios found were: infected seeds/infected seedlings 1:0.4, infected tillers/yield loss 1:0.9, infected seeds/yield loss 1:0.3. The threshold of seed infection at which production was not significantly different from the healthy control was 14%. Therefore seed treatment is advisable, under the conditions of Northern and Central Italy, when the percentage of seed infection in commercial seed lots is above this level. A tolerance near zero is recommended in prebasic and basic seeds. [ABSTRACT FROM AUTHOR]

Net form of net blotch (NFNB) caused by the fungus Pyrenophora teres f. teres is an economically important foliar disease of barley (Hordeum vulgare) in southern and eastern Africa. Little attention has been given to disease resistance breeding, and knowledge about the presence of NFNB resistance in breeding lines is limited. Deploying resistance into varieties used in this region is important for future control of the disease. We have identified NFNB disease resistance in existing South African breeders’ lines and have mapped the resistance in line UVC8. Six different trials, three conducted in South Africa and another three in Australia, were used to identify resistance QTL. A major QTL was identified on chromosome 6H having a LOD score of 40.5 and 55% of the phenotypic variance explained. Kompetitive Allele Specific PCR (KASP™) markers were designed for this QTL region. These and microsatellite markers can now be used to routinely select for NFNB resistance. [ABSTRACT FROM AUTHOR]