Evaluating the importance of the tan spot ToxA–Tsn1 interaction in Australian wheat varieties

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.     

Brachypodium distachyon is a pathosystem model for the study of the wheat disease rhizoctonia root rot

Brachypodium distachyon (Bd) is increasingly being used as a model for cereal diseases and to study cereal root architecture. Rhizoctonia solani AG 8 is a necrotrophic root pathogen that infects wheat soon after germination resulting in reduced plant growth and yield loss. Genetic resistance to R. solani AG 8 is not available in commercial wheat cultivars, although some quantitative levels of resistance have previously been found in mutant lines and grass relatives. Resistance mechanisms in cereals remain unknown. The ability to use Bd as a model to study the wheat–R. solani AG 8 pathosystem was investigated. The results presented show that Bd is susceptible to R. solani AG 8 and that the pathogen infects both species to a similar degree, producing comparable disease symptoms. Root length reduction was the primary indicator of disease, with shoots also affected. The second objective was to develop a repeatable phenotyping method to screen Bd populations for resistance to R. solani AG 8. Results of a preliminary experiment provide evidence for variation in resistance between Bd inbred lines. This is the first report showing the potential of Bd as a model plant for discovery of quantitative genetic variation in resistance to a necrotrophic cereal root pathogen.     

Host‐induced gene silencing in the necrotrophic fungal pathogen Sclerotinia sclerotiorum

Sclerotinia sclerotiorum is a necrotrophic fungus that causes a devastating disease called white mould, infecting more than 450 plant species worldwide. Control of this disease with fungicides is limited, so host plant resistance is the preferred alternative for disease management. However, due to the nature of the disease, breeding programmes have had limited success. A potential alternative to developing necrotrophic fungal resistance is the use of host‐induced gene silencing (HIGS) methods, which involves host expression of dsRNA‐generating constructs directed against genes in the pathogen. In this study, the target gene chosen was chitin synthase (chs), which commands the synthesis of chitin, the polysaccharide that is a crucial structural component of the cell walls of many fungi. Tobacco plants were transformed with an interfering intron‐containing hairpin RNA construct for silencing the fungal chs gene. Seventy‐two hours after inoculation, five transgenic lines showed a reduction in disease severity ranging from 55·5 to 86·7% compared with the non‐transgenic lines. The lesion area did not show extensive progress over this time (up to 120 h). Disease resistance and silencing of the fungal chs gene was positively correlated with the presence of detectable siRNA in the transgenic lines. It was demonstrated that expression of endogenous genes from the very aggressive necrotrophic fungus S. sclerotiorum could be prevented by host induced silencing. HIGS of the fungal chitin synthase gene can generate white mould‐tolerant plants. From a biotechnological perspective, these results open new prospects for the development of transgenic plants resistant to necrotrophic fungal pathogens.     

Early molecular signatures of responses of wheat to Zymoseptoria tritici in compatible and incompatible interactions

Zymoseptoria tritici, the causal agent of septoria tritici blotch, a serious foliar disease of wheat, is a necrotrophic pathogen that undergoes a long latent period. Emergence of insensitivity to fungicides, and pesticide reduction policies, mean there is a pressing need to understand septoria and control it through greater varietal resistance. Stb6 and Stb15, the most common qualitative resistance genes in modern wheat cultivars, determine specific resistance to avirulent fungal genotypes following a gene‐for‐gene relationship. This study investigated compatible and incompatible interactions of wheat with Z. tritici using eight combinations of cultivars and isolates, with the aim of identifying molecular responses that could be used as markers for disease resistance during the early, symptomless phase of colonization. The accumulation of TaMPK3 was estimated using western blotting, and the expression of genes implicated in gene‐for‐gene interactions of plants with a wide range of other pathogens was measured by qRT‐PCR during the presymptomatic stages of infection. Production of TaMPK3 and expression of most of the genes responded to inoculation with Z. tritici but varied considerably between experimental replicates. However, there was no significant difference between compatible and incompatible interactions in any of the responses tested. These results demonstrate that the molecular biology of the gene‐for‐gene interaction between wheat and Zymoseptoria is unlike that in many other plant diseases, indicate that environmental conditions may strongly influence early responses of wheat to infection by Z. tritici, and emphasize the importance of including both compatible and incompatible interactions when investigating the biology of this complex pathosystem.     

Mining the Watkins collection of wheat landraces for novel sources of eyespot resistance

Eyespot is an economically important stem base disease of wheat caused by the soilborne fungal pathogens Oculimacula yallundae and Oculimacula acuformis. The most effective method of controlling the disease is host resistance. However, there are only three genetically characterized resistances in wheat varieties and further sources of resistance are required. Previous studies have identified resistances in wild relatives, but use of these resistances has been limited by linkage drag with deleterious traits exacerbated by low rates of recombination. Therefore, the identification of novel resistances in hexaploid wheat germplasm is desirable. The Watkins collection currently consists of 1056 hexaploid wheat landraces that represent global wheat diversity at the time of its collection in the 1920s and 1930s. As such, it may contain beneficial agronomic traits such as eyespot resistance. The Watkins collection was screened for resistance to O. yallundae based on a glasshouse test of all 1056 accessions and a polytunnel test of 44 accessions selected from a previous field trial. Resistant lines identified in these tests were retested against both O. yallundae and O. acuformis. This identified 17 accessions with resistance to one or both of the pathogen species. From these, two accessions (1190094.1 and 1190736.3) provided a high level of resistance to both pathogen species. An F₄ population derived from accession 1190736.3 indicated that the resistance to O. acuformis in this accession is conferred by a single gene and therefore would be suitable for introgression into elite wheat varieties to provide an alternative source of eyespot resistance.     

Effect of azole fungicide mixtures,alternations and dose on azole sensitivity in the wheat pathogen Zymoseptoria tritici

The evolution of fungicide resistance in the cereal pathogen Zymoseptoria tritici is a serious threat to the sustainability and profitability of wheat production in Europe. Application of azole fungicides has been shown to affect fitness of Z. tritici variants differentially, so it has been hypothesized that combinations of azoles could slow the evolution of resistance. This work assessed the effects of dose, mixtures and alternations of two azoles on selection for isolates with reduced sensitivity and on disease control. Naturally infected field trials were carried out at six sites across Ireland and the sensitivity of Z. tritici isolates monitored pre‐ and post‐treatment. Epoxiconazole and metconazole were applied as solo products, in alternation with each other, and as a pre‐formulated mixture. Full and half label doses were tested. Isolates were partially cross‐resistant to the two azoles, with a common azole resistance principal component accounting for 75% of the variation between isolates. Selection for isolates with reduced azole sensitivity was correlated with disease control. Decreased doses were related to decreases in sensitivity but the effect was barely significant (P = 0·1) and control was reduced. Single applications of an active ingredient (a.i.) caused smaller decreases in sensitivity than double applications. Shifts in sensitivity to the a.i. applied to a plot were greater than to the a.i. not applied, and the decrease in sensitivity was greater to the a.i. applied at the second timing. These results confirm the need to mix a.i.s with different modes of action.     

Novel necrotrophic effectors from Stagonospora nodorum and corresponding host sensitivities in winter wheat germplasm in the southeastern United States

Stagonospora nodorum blotch (SNB), caused by the necrotrophic fungus Stagonospora nodorum (teleomorph: Phaeosphaeria nodorum), is among the most common diseases of winter wheat in the United States. New opportunities in resistance breeding have arisen from the recent discovery of several necrotrophic effectors (NEs, also known as host-selective toxins) produced by S. nodorum, along with their corresponding host sensitivity (Snn) genes. Thirty-nine isolates of S. nodorum collected from wheat debris or grain from seven states in the southeastern United States were used to investigate the production of NEs in the region. Twenty-nine cultivars with varying levels of resistance to SNB, representing 10 eastern-U.S. breeding programs, were infiltrated with culture filtrates from the S. nodorum isolates in a randomized complete block design. Three single-NE Pichia pastoris controls, two S. nodorum isolate controls, and six Snn-differential wheat controls were also used. Cultivar-isolate interactions were visually evaluated for sensitivity at 7 days after infiltration. Production of NEs was detected in isolates originating in each sampled state except Maryland. Of the 39 isolates, 17 produced NEs different from those previously characterized in the upper Great Plains region. These novel NEs likely correspond to unidentified Snn genes in Southeastern wheat cultivars, because NEs are thought to arise under selection pressure from genes for resistance to biotrophic pathogens of wheat cultivars that differ by geographic region. Only 3, 0, and 23% of the 39 isolates produced SnToxA, SnTox1, and SnTox3, respectively, by the culture-filtrate test. A Southern dot-blot test showed that 15, 74, and 39% of the isolates carried the genes for those NEs, respectively; those percentages were lower than those found previously in larger international samples. Only two cultivars appeared to contain known Snn genes, although half of the cultivars displayed sensitivity to culture filtrates containing unknown NEs. Effector sensitivity was more frequent in SNB-susceptible cultivars than in moderately resistant (MR) cultivars (P = 0.008), although some susceptible cultivars did not exhibit sensitivity to NEs produced by isolates in this study and some MR cultivars were sensitive to NEs of multiple isolates. Our results suggest that NE sensitivities influence but may not be the only determinant of cultivar resistance to S. nodorum. Specific knowledge of NE and Snn gene frequencies in this region can be used by wheat breeding programs to improve SNB resistance.     

Genetic architecture of adult plant resistance to leaf rust in a wheat association mapping panel

Leaf rust caused by Puccina triticina is one of the most destructive fungal diseases of wheat (Triticum aestivum). Adult plant resistance (APR) is an effective strategy to achieve long‐term protection from the disease. In this study, findings are reported from a genome‐wide association study (GWAS) using a panel of 96 wheat cultivars genotyped with 874 Diversity Arrays Technology (DArT) markers and tested for adult leaf rust response in six field trials. A total of 13 quantitative trait loci (QTL) conferring APR to leaf rust were identified on chromosome arms 1BL, 1DS, 2AS, 2BL, 2DS, 3BS, 3BL, 4AL, 6BS (two), 7DS, 5BL/7BS and 6AL/6BS. Of these, seven QTLs mapped close to known resistance genes and QTLs, while the remaining six are novel and can be used as additional sources of resistance. Accessions with a greater number of combined QTLs for APR showed lower levels of disease severity, demonstrating additive and significant pyramiding effects. All QTLs had stable main effects and they did not exhibit a significant interaction with the experiments. These findings could help to achieve adequate levels of durable resistance through marker‐assisted selection and pyramiding resistance QTLs in local germplasm.     

Cultivar‐dependent partial resistance and associated defence mechanisms in wheat against Zymoseptoria tritici

Septoria tritici blotch caused by the fungus Zymoseptoria tritici is one of the most devastating foliar diseases of wheat. Knowledge regarding mechanisms involved in resistance against this disease is required to breed durable resistances. This study compared the expression of defence and pathogenicity determinants in three cultivars in semicontrolled culture conditions. The most susceptible cultivar, Alixan, presented higher necrosis and pycnidia density levels than Altigo, the most resistant one. In Premio, a moderately resistant cultivar, necrosis developed as in Alixan, while pycnidia developed as in Altigo. In noninfectious conditions, genes coding for PR1 (pr1), glucanase (gluc) and allene oxide synthase (aos) were constitutively expressed at a higher level in both Altigo and Premio than in Alixan, while chitinase2 (chit2), phenylalanine ammonia‐lyase (pal), peroxidase (pox2) and oxalate oxidase (oxo) were expressed at a higher level in Premio only. Except for aos, all genes were induced in Alixan during the first steps of the symptomless infection phase. Only pox2, oxo, gluc and pal genes in Altigo and pal, chs and lox genes in Premio were up‐regulated at some time points. Basal cultivar‐dependent resistance against Z. tritici could therefore be explained by various gene expression patterns rather than high expression levels of given genes. During the necrotrophic phase, Z. tritici cell wall‐degrading enzyme activity levels were lower in Altigo and Premio than in Alixan, and were associated more with pycnidia than with necrosis. Similar tissue colonization occurred in the three cultivars, suggesting an inhibition of the switch to the necrotrophic lifestyle in Altigo.     

Resistance to Xanthomonas perforans race T4 causing bacterial spot in tomato breeding lines

Tomato (Solanum lycopersicum) is the second most important vegetable crop in the world. Bacterial spot (BS) of tomato, caused by four species of Xanthomonas: X. euvesicatoria, X. vesicatoria, X. perforans and X. gardneri, results in severe loss in yield and quality due to defoliation and formation of lesions on fruits, respectively. Currently management practices do not offer effective control under conditions of high disease pressure. Thus, developing BS resistance is a critical priority for tomato growers in order to minimize crop losses. Sixty‐three advanced tomato breeding lines, heirlooms and wild tomato lines with diverse genetic backgrounds were screened under greenhouse and field conditions for BS resistance using X. perforans race T4, which was found to be a prevalent race in North Carolina. Race T4 isolate 9 was used to inoculate the plants by spraying, and disease severity was measured using the Horsfall–Barratt scale. Tomato lines 74L‐1W(2008), NC2CELBR, 081‐12‐1X‐gsms, NC22L‐1 (2008) and 52LB‐1 showed resistance to BS in the field and/or greenhouse trials. These lines were derived from S. pimpinellifolium L3707. Screening L3707 followed by development of a mapping population and mapping resistance genes might be useful for breeding resistance against BS in future breeding programmes.     

SnToxA,SnTox1, and SnTox3 originated in Parastagonospora nodorum in the Fertile Crescent

The centre of origin of the globally distributed wheat pathogen Parastagonospora nodorum has remained uncertain because only a small number of isolates from the Fertile Crescent were included in earlier population genetic and phylogeographic studies. We isolated and genetically analysed 193 P. nodorum strains from three naturally infected wheat fields distributed across Iran using 11 neutral microsatellite loci. Compared to previous studies that included populations from North America, Europe, Africa, Australia, and China, the populations from Iran had the highest genetic diversity globally and also exhibited greater population structure over smaller spatial scales, patterns typically associated with the centre of origin of a species. Genes encoding the necrotrophic effectors SnToxA, SnTox1, and SnTox3 were found at a high frequency in the Iranian population. By sequencing 96 randomly chosen Iranian strains, we detected new alleles for all three effector genes. Analysis of allele diversity showed that all three effector genes had higher diversity in Iran than in any population included in previous studies, with Iran acting as a hub for the effector diversity that was found in other global populations. Taken together, these findings support the hypothesis that P. nodorum originated either within or nearby the Fertile Crescent with a genome that already encoded all three necrotrophic effectors during its emergence as a pathogen on wheat. Our findings also suggest that P. nodorum was the original source of the ToxA genes discovered in the wheat pathogens Phaeosphaeria avenaria f. sp. tritici 1, Pyrenophora tritici-repentis, and Bipolaris sorokiniana.     

Winter annual grassy weeds increase over‐winter mortality in autumn‐sown wheat

Over‐winter mortality, that is, winterkill, reduces cereal crop competitive ability and yield. While management and environmental variables are known to affect winterkill, the extent to which weeds contribute to increased winterkill is largely unknown. Winter annual weeds may increase winterkill through resource competition and by increasing incidence of and damage from plant pathogens that cause winterkill. We evaluated the impact of summer annual (Avena fatua) and winter annual (Bromus tectorum) weeds on the over‐winter survival rate of winter wheat over three winters, during which plots were covered with snow. Pink snow mould (Microdochium nivale), a winterkill pathogen known to infect B. tectorum and winter wheat, was common in wheat stands. In weed‐free treatments, mortality rates were initially near zero, but increased by nearly 45% in each subsequent winter, presumably due to an increase in snow mould disease in continuously cropped winter wheat. Whereas A. fatua infestation had no impact on crop survival rates, winter wheat survival in B. tectorum‐infested plots was 50% less than the weed‐free control in the second and third years of this study. Among B. tectorum‐infested plots, winter wheat over‐winter survival declined with increasing weed seed produced in the previous summer. Overall, this study demonstrated that winter annual weed infestations can reduce crop stand densities below replanting thresholds by reducing fall‐sown cereal winter survival. The effects of winter annual weeds on winter wheat may be meditated by increased proliferation of snow mould disease.     

Effect of wheat spike infection timing on fusarium head blight development and mycotoxin accumulation

Fusarium head blight in wheat spikes is associated with production of mycotoxins by the fungi. Although flowering is recognized as the most favourable host stage for infection, a better understanding of infection timing on disease development and toxin accumulation is needed. This study monitored the development of eight characterized isolates of F. graminearum, F. culmorum and F. poae in a greenhouse experiment. The fungi were inoculated on winter wheat spikes before or at anther extrusion, or at 8, 18 and 28 days later. Disease levels were estimated by the AUDPC and thousand‐kernel weight (TKW). The fungal biomass (estimated by qPCR) and toxin concentration (deoxynivalenol and nivalenol, estimated by UPLC‐UV‐MS/MS) were measured in each inoculated spike, providing a robust estimation of these variables and allowing correlations based on single‐individual measurements to be established. The toxin content correlated well with fungal biomass in kernels, independently of inoculation date. The AUDPC was correlated with fungal DNA, but not for early and late infection dates. The highest disease and toxin levels were for inoculations around anthesis, but early or late infections led to detectable levels of fungus and toxin for the most aggressive isolates. Fungal development appeared higher in kernels than in the chaff for inoculations at anthesis, but the opposite was found for later inoculations. These results show that anthesis is the most susceptible stage for FHB, but also clearly shows that early and late infections can produce significant disease development and toxin accumulation with symptoms difficult to estimate visually.     

Resistance to Oculimacula yallundae and Oculimacula acuformis is conferred by Pch2 in wheat

The recent report of a differential response of wheat lines containing the Pch2 gene to infection with the eyespot pathogens Oculimacula yallundae and O. acuformis has prompted this re‐examination of the response to these fungi by the recombinant lines used to map Pch2. Homozygous recombinant substitution lines (RSL) derived from the hybridization of Chinese Spring (CS) and the CS chromosome substitution line Cappelle Desprez 7A (CS/CD7A), previously evaluated for response to glucuronidase (GUS)‐transformed O. yallundae, were evaluated for response to infection with GUS‐transformed O. acuformis. Based on visual scores and on GUS expression level, which reflects fungal colonization of seedling plants, evidence of a quantitative trait locus (QTL) conferring resistance to O. acuformis was found in two separate growth chamber experiments (logarithm of the odds, LOD, = 2·7 and 6·7 at 305 and 289 cM, respectively) that was equivalent in location to that for resistance to O. yallundae (LOD = 13·2 and 11·4 at 289 and 304 cM, respectively). These results confirm that Pch2 confers some degree of resistance against both O. yallundae and O. acuformis under these conditions.     

Genetic analysis and molecular mapping of resistance to Puccinia striiformis f. sp. pseudo‐hordei in common wheat

This is the first genetic study reporting on the interaction and molecular mapping of resistance to the barley grass stripe rust pathogen (Puccinia striiformis f. sp. pseudo‐hordei, Psph) in common wheat. Seedlings of 638 wheat accessions were tested and it was determined that wheat is a near‐nonhost to Psph based on rare susceptibility observed in <2% of commercial cultivars and <5% of wheat landraces. As previously observed for P. striiformis f. sp. tritici (Pst), the Australian cultivar Teal was highly susceptible to Psph. In contrast, a selection of cv. Avocet carrying complementary resistance genes Yr73 and Yr74 (Avocet R; AvR) was resistant. The Teal × AvR (T/A) doubled haploid (DH) population was used to map resistance in AvR to Psph. Infection types on the T/A DH lines inoculated with Psph and Pst indicated that all DH lines carrying both Yr73 and Yr74 were also resistant to Psph; however, fewer DH lines were susceptible to Psph than expected, suggesting the resistance was more complex. QTL analysis using 9053 DArT‐Seq markers determined that resistance to Psph was polygenically inherited and mapped to chromosomes 3A, 3D, 4A and 5B. The 3DL and 5BL markers co‐located with Yr73 and Yr74, suggesting an overlap between host and non‐host resistance mechanisms.     

Effects of blast on components of wheat physiology and grain yield as influenced by fungicide treatment and host resistance

Two field experiments (Exp. 1 and Exp. 2) were carried out to assess the physiological performance and grain yield of wheat cultivars BR‐18 (moderately resistant) and Guamirim (susceptible) inoculated with Pyricularia oryzae in plots treated or untreated with Ópera (fungicide 13.3% epoxiconazole + 5% pyraclostrobin). Results from regression analyses indicated that spike and leaf blast severity at 10–14 days after inoculation (dai) were associated with greater yield losses (highest negative slope) than severity at 18–22 dai. Relative to untreated Guamirim, there were 0.3% and 16% increases in Exp. 1 and 2, respectively, for untreated BR‐18 (resistance alone). For fungicide treatment alone, the mean yield of Guamirim increased by 20% and 61% in Exp. 1 and 2, respectively, relative to the untreated fungicide control, whereas for the fungicide treated BR‐18, the mean yield increased by 26% and 83% in Exp. 1 and 2, respectively. Fungicide application and cultivar resistance resulted in higher measures of leaf health and photosynthetic performance in both spikes and leaves than in the untreated susceptible reference treatment. The results from this study may be useful in future efforts to develop crop loss models and management guidelines for wheat blast.     

Diversity of Avr‐vnt1 and AvrSmira1 effector genes in Polish and Norwegian populations of Phytophthora infestans

The oomycete Phytophthora infestans, the cause of late blight, is one of the most important potato pathogens. During infection, it secretes effector proteins that manipulate host cell function, thus contributing to pathogenicity. This study examines sequence differentiation of two P. infestans effectors from 91 isolates collected in Poland and Norway and five reference isolates. A gene encoding the Avr‐vnt1 effector, recognized by the potato Rpi‐phu1 resistance gene product, is conserved. In contrast, the second effector, AvrSmira1 recognized by Rpi‐Smira1, is highly diverse. Both effectors contain positively selected amino acids. A majority of the polymorphisms and all selected sites are located in the effector C‐terminal region, which is responsible for their function inside host cells. Hence it is concluded that they are associated with a response to diversified target protein or recognition avoidance. Diversification of the AvrSmira1 effector sequences, which existed prior to the large‐scale cultivation of plants containing the Rpi‐Smira1 gene, may reduce the predicted durability of resistance provided by this gene. Although no isolates virulent to plants with the Rpi‐phu1 gene were found, the corresponding Avr‐vnt1 effector has undergone selection, providing evidence for an ongoing ‘arms race’ between the host and pathogen. Both genes remain valuable components for resistance gene pyramiding.     

Measuring lesion attributes and analysing their spatial patterns at the leaf scale using digital image analysis

Digital image analysis was used to quantify size, shape and relative positions of individual plant disease lesions to determine their spatial distribution pattern at the leaf scale. Rice brown spot was used as a necrotrophic pathogen causing numerous discrete lesions. A 50‐leaf subsample was selected from an existing data set of 350 images of leaves taken from the field, and analysed for disease severity using image analysis. Further measurements included size, shape and the relative positions of lesions for all leaves with severity > 8% (n = 25) and an additional 25‐leaf sample with severity <8%. A total of 3964 necrotic and/or halo areas were selected using a manually defined threshold in the computer program Assess . There were significant and positive associations (Pearson's r > 0.81; P < 0.001) between the size‐related measurements (lesion area, longest and shortest axis). Coalesced areas, formed by interconnection of lesions and associated haloes, and a high number of small lesions were found with an increase in severity, suggesting a secondary cycle and autoinfection process. Results from quadrat‐based (Poisson distribution and Spatial Analysis by Distance IndicEs) and distance‐based (point‐process Poisson) spatial methods were in good agreement and, together with a Taylor power law model, suggested a shift from random to predominantly aggregated patterns of lesions at severities approaching 10%. This framework, which is applicable to other foliar diseases, proved useful in providing quantitative knowledge of epidemic processes at the leaf scale. Finally, these results may be useful in improving simulation models and disease assessment methods.     

Biology and control of cephalosporium stripe of wheat

Cephalosporium stripe, caused by the fungus Cephalosporium gramineum, is the only known vascular wilt disease of small grain cereals. The pathogen causes characteristic striping of leaf blades and sheaths, but can also result in seedling death, stunting, and sterile seed heads (white heads). Cephalosporium stripe is a disease of autumn (fall)‐sown wheat, especially in cool and wet production regions. The disease is further favoured by early sowing, reduced tillage practices, low pH soils, and by frost heaving that damages roots. Infections occur almost entirely from spores produced on surface crop debris that are washed into the soil, although a low level of seed transmission can also occur. The pathogen colonizes root epidermis and cortical cells, subsequently moves into the vascular tissue, and eventually spreads throughout the entire plant. Production of fungal toxin(s) and extracellular polysaccharides probably play an important role in pathogenesis. Cultural practices such as delayed sowing, crop rotation, destruction of crop debris, liming of soil and fertilizer management all have potential to reduce the incidence of cephalosporium stripe. All of these cultural practices have negative economic impacts and/or increase soil erosion, and thus there is much interest in the development of resistant cultivars. There is potential for introgression of highly effective resistance from wild species into cultivated wheat. Genes for quantitatively inherited resistance can also be accumulated within cultivated wheat to attain moderate resistance. The continued use of cultivars with moderate resistance will probably be sufficient for long‐term control of the disease.     

Virulence and toxin synthesis of an azole insensitive Fusarium culmorum strain in wheat cultivars with different levels of resistance to fusarium head blight

Fusarium culmorum causes head blight, produces toxins and reduces yield and quality of cereals. To prevent damage caused by fusarium head blight (FHB), azole fungicides are mainly applied. The occurrence of insensitivity to azoles is a major problem in agriculture. The present study shows that a tebuconazole insensitive strain of F. culmorum can be readily produced in the laboratory, but that the resulting strain of the fungus is of lower fitness in vitro. Insensitivity was confirmed microscopically and by cell viability and metabolic activity. The tebuconazole insensitive strain shows cross insensitivity to nine important azoles. In addition, plants inoculated with the insensitive F. culmorum strain showed no reduction of FHB symptoms and deoxynivalenol (DON) content after tebuconazole treatment, compared to an inoculation with the sensitive strain. Use of wheat cultivars carrying a high resistance level (i.e. cv. Toras) was the most effective method for reducing symptoms and decreasing DON content, independent from the level of fungicide insensitivity of the F. culmorum strain. In conclusion, resistant cultivars and a fungicide mixture which combines different mechanisms of action in fungal metabolism should be applied to avoid fungicide insensitivity of Fusarium spp. in future.