Identification of Quantitative Trait Loci for Resistance to Wheat Sharp Eyespot in the Einstein × Tubbs Recombinant Inbred Line Population.

Wheat sharp eyespot (SES), caused by the soilborne pathogen Rhizoctonia cerealis Van der Hoeven (teleomorph: Ceratobasidium cereale), is a common stem disease of wheat globally. The disease caused a severe and extensive epidemic throughout the Willamette Valley of Oregon in 2014 and has remained one of the most important wheat diseases in this region. However, little was known about the genetics of host resistance to this disease. A recombinant inbred line (RIL) population with 257 lines developed from a cross of Einstein × Tubbs was used to study SES resistance of wheat. The phenotyping was conducted at two locations and in 3 years. Genotyping by sequencing was done by using Illumina HiSeq 3000. Low broad-sense heritability across four environments was obtained. The results of analysis of variance demonstrated that disease severity was significantly different among RILs for the data combined over environments and for one of the individual environments. Four SES resistance quantitative trait loci (QTL) were detected, including QSES-1A, QSES-2B, QSES-6A, and QSES-7A, and explained 5.9, 5.9, 8.8, and 8.3%, respectively, of the phenotypic variance. All four QTL overlapped or are in close proximity with one or more plant defense genes, and could lay the foundation for marker-assisted breeding.

Delays in Epidemic Outbreak Control Cost Disproportionately Large Treatment Footprints to Offset.

Epidemic outbreak control often involves a spatially explicit treatment area (quarantine, inoculation, ring cull) that covers the outbreak area and adjacent regions where hosts are thought to be latently infected. Emphasis on space however neglects the influence of treatment timing on outbreak control. We conducted field and in silico experiments with wheat stripe rust (WSR), a long-distance dispersed plant disease, to understand interactions between treatment timing and area interact to suppress an outbreak. Full-factorial field experiments with three different ring culls (outbreak area only to a 25-fold increase in treatment area) at three different disease control timings (1.125, 1.25, and 1.5 latent periods after initial disease expression) indicated that earlier treatment timing had a conspicuously greater suppressive effect than the area treated. Disease spread computer simulations over a broad range of influential epidemic parameter values (R0, outbreak disease prevalence, epidemic duration) suggested that potentially unrealistically large increases in treatment area would be required to compensate for even small delays in treatment timing. Although disease surveillance programs are costly, our results suggest that treatments early in an epidemic disease outbreak require smaller areas to be effective, which may ultimately compensate for the upfront costs of proactive disease surveillance programs.

Comparing the efficacy of control strategies for infectious disease outbreaks using field and simulation studies.

Diseases characterized by long distance inoculum dispersal (LDD) are among the fastest spreading epidemics in both natural and managed landscapes. Management of such epidemics is extremely challenging because of asymptomatic infection extending at large spatial scales and frequent escape from the newly established disease sources. We compared the efficacy of area- and timing-based disease management strategies in artificially initiated field epidemics of wheat stripe rust and complemented with simulations from an updated version of the spatially explicit model EPIMUL, using model parameters relevant to field epidemics. The model was further used to expand the number of epidemic mitigations beyond that feasible to incorporate in the field. The field experiment was conducted for 2 years in two locations having different climatic conditions. Culling and protection treatments were applied at different times after epidemic initiation and to different spatial extents surrounding the outbreaks. In each experiment, treatments were replicated four times in plots 33.5 m long and 1.52 m wide with a 0.76 × 0.76 m inoculated focus centered within each plot. Disease gradients were assessed along the center lines of the plots at 1.52 m intervals both upwind and downwind from the focus. Both field and simulation results indicated that control measures applied over the entire population were highly effective in suppressing the epidemics by more than 99% but may not always be logistically and economically feasible at large spatial scales. Comparison between the variable sized treatment areas and application timings suggested that implementing contiguous premises (CP) cull at 1 day after first sporulation in the outbreak focus reduced rust by 52% and 60% in Corvallis and Madras, respectively. However, altering the cull size did not significantly affect the disease epidemic development, which suggested that early timing had a greater influence in suppressing the epidemics than did increased area of application. However, sufficiently large, treated areas may compensate for a delay in application timing to some extent. Results from these replicated treatments may help to devise appropriate management strategies for other LDD pathogens.

Baseline and Temporal Changes in Sensitivity of Zymoseptoria tritici Isolates to Benzovindiflupyr in Oregon, U.S.A., and Cross-Sensitivity to Other SDHI Fungicides.

Zymoseptoria tritici is the causal agent of Septoria tritici blotch (STB), a disease of wheat (Triticum aestivum) that results in significant yield loss worldwide. Z. tritici's life cycle, reproductive system, effective population size, and gene flow put it at high likelihood of developing fungicide resistance. Succinate dehydrogenase inhibitor (SDHI) fungicides (FRAC code 7) were not widely used to control STB in the Willamette Valley until 2016. Field isolates of Z. tritici collected in the Willamette Valley at dates spanning the introduction of SDHI (2015 to 2017) were screened for sensitivity to four SDHI active ingredients: benzovindiflupyr, penthiopyrad, fluxapyroxad, and fluindapyr. Fungicide sensitivity changes were determined by the fungicide concentration at which fungal growth is decreased by 50% (EC50) values. The benzovindiflupyr EC50 values increased significantly, indicating a reduction in sensitivity, following the adoption of SDHI fungicides in Oregon (P < 0.0001). Additionally, significant reduction in cross-sensitivity among SDHI active ingredients was also observed with a moderate and significant relationship between penthiopyrad and benzovindiflupyr (P = 0.0002) and a weak relationship between penthiopyrad and fluxapyroxad (P = 0.0482). No change in cross-sensitivity was observed with fluindapyr, which has not yet been labeled in the region. The results document a decrease in SDHI sensitivity in Z. tritici isolates following the introduction of the active ingredients to the Willamette Valley. The reduction in cross-sensitivity observed between SDHI active ingredients highlights the notion that careful consideration is required to manage fungicide resistance and suggests that within-group rotation is insufficient for resistance management.

Methods for Screening Wheat Genotypes for Resistance to Sharp Eyespot in the Field and Greenhouse.

Screening methodology of wheat genotypes for resistance to sharp eyespot (caused by Rhizoctonia cerealis) was developed. Disease severity differed among cultivars and between field and greenhouse trials. However, the cultivars Bobtail and Rosalyn had consistently lower severity in field experiments with high sharp eyespot disease pressure. Artificial inoculation was crucial to achieving adequate disease levels for effective screening but planting date had very little effect. Greenhouse inoculation of adult wheat plants was much less successful in categorizing resistance to sharp eyespot. Seedling inoculations in the greenhouse were highly inadequate as a screening method. Selection for resistance to sharp eyespot by artificial inoculation in field trials is feasible in wheat breeding programs.

Dispersal Kernels may be Scalable: Implications from a Plant Pathogen.

AIM: Understanding how spatial scale of study affects observed dispersal patterns can provide insights into spatiotemporal population dynamics, particularly in systems with significant long-distance dispersal (LDD). We aimed to investigate the dispersal gradients of two rusts of wheat with spores of similar size, mass, and shape, over multiple spatial scales. We hypothesized that a single dispersal kernel could fit the dispersal from all spatial scales well, and that it would be possible to obtain similar results in spatiotemporal increase of disease when modeling based on differing scales. LOCATION: Central Oregon and St. Croix Island. TAXA: Puccinia striiformis f. sp. tritici, Puccinia graminis f. sp. tritici, Triticum aestivum. METHODS: We compared empirically-derived primary disease gradients of cereal rust across three spatial scales: local (inoculum source and sampling unit = 0.0254 m, spatial extent = 1.52m) field-wide (inoculum source = 1.52 m, sampling unit = 0.305 m, and spatial extent = 91.44 m), and regional (inoculum source and sampling unit = 152 m, spatial extent = 10.7 km). We then examined whether disease spread in spatially explicit simulations depended upon the scale at which data were collected by constructing a compartmental time-step model. RESULTS: The three data sets could be fit well by a single inverse-power law dispersal kernel. Simulating epidemic spread at different spatial resolutions resulted in similar patterns of spatiotemporal spread. Dispersal kernel data obtained at one spatial scale can be used to represent spatiotemporal disease spread at a larger spatial scale. MAIN CONCLUSIONS: Organisms spread by aerially dispersed small propagules that exhibit LDD may follow similar dispersal patterns over a several hundred- or thousand-fold expanse of spatial scale. Given that the primary mechanisms driving aerial dispersal remain constant, it may be possible to extrapolate across scales when empirical data are unavailable at a scale of interest.

Consequences of Long-Distance Dispersal for Epidemic Spread: Patterns, Scaling, and Mitigation.

Epidemics caused by long-distance dispersed pathogens result in some of the most explosive and difficult to control diseases of both plants and animals (including humans). Yet the factors influencing disease spread, especially in the early stages of the outbreak, are not well-understood. We present scaling relationships, of potentially widespread relevance, that were developed from more than 15 years of field and in silico single focus studies of wheat stripe rust spread. These relationships emerged as a consequence of accounting for a greater proportion of the fat-tailed disease gradient that may be frequently underestimated in disease spread studies. Leptokurtic dispersal gradients (highly peaked and fat-tailed) are relatively common in nature and they can be represented by power law functions. Power law scale invariance properties generate patterns that repeat over multiple spatial scales, suggesting important and predictable scaling relationships between disease levels during the first generation of disease outbreaks and subsequent epidemic spread. Experimental wheat stripe rust outbreaks and disease spread simulations support theoretical scaling relationships from power law properties and suggest that relatively straightforward scaling approximations may be useful for projecting the spread of disease caused by long-distance dispersed pathogens. Our results suggest that, when actual dispersal/disease data are lacking, an inverse power law with exponent = 2 may provide a reasonable approximation for modeling disease spread. Furthermore, our experiments and simulations strongly suggest that early control treatments with small spatial extent are likely to be more effective at suppressing an outbreak caused by a long-distance dispersed pathogen than would delayed treatment of a larger area. The scaling relationships we detail and the associated consequences for disease control may be broadly applicable to plant and animal pathogens characterized by non-exponentially bound, fat-tailed dispersal gradients.

Pyramiding for Resistance Durability: Theory and Practice.

Durable disease resistance is a key component of global food security, and combining resistance genes into "pyramids" is an important way to increase durability of resistance. The mechanisms by which pyramids impart durability are not well known. The traditional view of resistance pyramids considers the use of major resistance gene (R-gene) combinations deployed against pathogens that are primarily asexual. Interestingly, published examples of the successful use of pyramids in the traditional sense are rare. In contrast, most published descriptions of durable pyramids in practice are for cereal rusts, and tend to indicate an association between durability and cultivars combining major R-genes with incompletely expressed, adult plant resistance genes. Pyramids have been investigated experimentally for a diversity of pathogens, and many reduce disease levels below that of the single best gene. Resistance gene combinations have been identified through phenotypic reactions, molecular markers, and challenge against effector genes. As resistance genes do not express equally in all genetic backgrounds, however, a combination of genetic information and phenotypic analyses provide the ideal scenario for testing of putative pyramids. Not all resistance genes contribute equally to pyramids, and approaches have been suggested to identify the best genes and combinations of genes for inclusion. Combining multiple resistance genes into a single plant genotype quickly is a challenge that is being addressed through alternative breeding approaches, as well as through genomics tools such as resistance gene cassettes and gene editing. Experimental and modeling tests of pyramid durability are in their infancy, but have promise to help direct future studies of pyramids. Several areas for further work on resistance gene pyramids are suggested.

Variable competitive effects of fungicide resistance in field experiments with a plant pathogenic fungus.

Classic evolutionary theory suggests that mutations associated with antimicrobial and pesticide resistance result in a fitness cost in the absence of the selective antimicrobial agent or pesticide. There is experimental evidence to support fitness costs associated with resistance to anti-microbial compounds and pesticides across many biological disciplines, including human pathology, entomology, plant sciences, and plant pathology. However, researchers have also found examples of neutral and increased fitness associated with resistance, where the effect of a given resistance mutation depends on environmental and biological factors. We used Zymoseptoria tritici, a model evolutionary plant pathogenic fungus, to compare the competitive ability of fungicide-resistant isolates to fungicide-sensitive isolates. We conducted four large-scale inoculated winter wheat experiments at Oregon State University agriculture experiment stations. We found a significant change in the frequency of fungicide resistance over time in all four experiments. The direction and magnitude of these changes, however, differed by experimental location, year of experiment, and inoculum resistance treatment (fungicide-resistant, resistant/sensitive mixture, and fungicide-sensitive). These results suggest that the competitive ability of resistant isolates relative to sensitive isolates varied depending upon environmental conditions, including the initial frequency of resistant individuals in the population.

Cropping system diversification for food production in Mindanao rubber plantations: a rice cultivar mixture and rice intercropped with mungbean.

Including food production in non-food systems, such as rubber plantations and biofuel or bioenergy crops, may contribute to household food security. We evaluated the potential for planting rice, mungbean, rice cultivar mixtures, and rice intercropped with mungbean in young rubber plantations in experiments in the Arakan Valley of Mindanao in the Philippines. Rice mixtures consisted of two- or three-row strips of cultivar Dinorado, a cultivar with higher value but lower yield, and high-yielding cultivar UPL Ri-5. Rice and mungbean intercropping treatments consisted of different combinations of two- or three-row strips of rice and mungbean. We used generalized linear mixed models to evaluate the yield of each crop alone and in the mixture or intercropping treatments. We also evaluated a land equivalent ratio for yield, along with weed biomass (where Ageratum conyzoides was particularly abundant), the severity of disease caused by Magnaporthe oryzae and Cochliobolus miyabeanus, and rice bug (Leptocorisa acuta) abundance. We analyzed the yield ranking of each cropping system across site-year combinations to determine mean relative performance and yield stability. When weighted by their relative economic value, UPL Ri-5 had the highest mean performance, but with decreasing performance in low-yielding environments. A rice and mungbean intercropping system had the second highest performance, tied with high-value Dinorado but without decreasing relative performance in low-yielding environments. Rice and mungbean intercropped with rubber have been adopted by farmers in the Arakan Valley.

Temporal Dynamics and Spatial Variation of Azoxystrobin and Propiconazole Resistance in Zymoseptoria tritici: A Hierarchical Survey of Commercial Winter Wheat Fields in the Willamette Valley, Oregon.

Fungicide resistance can cause disease control failure in agricultural systems, and is particularly concerning with Zymoseptoria tritici, the causal agent of Septoria tritici blotch of wheat. In North America, the first quinone outside inhibitor resistance in Z. tritici was discovered in the Willamette Valley of Oregon in 2012, which prompted this hierarchical survey of commercial winter wheat fields to monitor azoxystrobin- and propiconazole-resistant Z. tritici. Surveys were conducted in June 2014, January 2015, May 2015, and January 2016. The survey was organized in a hierarchical scheme: regions within the Willamette Valley, fields within the region, transects within the field, and samples within the transect. Overall, frequency of azoxystrobin-resistant isolates increased from 63 to 93% from June 2014 to January 2016. Resistance to azoxystrobin increased over time even within fields receiving no strobilurin applications. Propiconazole sensitivity varied over the course of the study but, overall, did not significantly change. Sensitivity to both fungicides showed no regional aggregation within the Willamette Valley. Greater than 80% of spatial variation in fungicide sensitivity was at the smallest hierarchical scale (within the transect) of the survey for both fungicides, and the resistance phenotypes were randomly distributed within sampled fields. Results suggest a need for a better understanding of the dynamics of fungicide resistance at the landscape level.

Invasiveness of plant pathogens depends on the spatial scale of host distribution.

Plant diseases often cause serious yield losses in agriculture. A pathogen's invasiveness can be quantified by the basic reproductive number, R0. Since pathogen transmission between host plants depends on the spatial separation between them, R0 is strongly influenced by the spatial scale of the host distribution. We present a proof of principle of a novel approach to estimate the basic reproductivenumber, R0, of plant pathogens as a function of the size of a field planted with crops and its aspect ratio. This general approach is based on a spatially explicit population dynamical model. The basic reproductive number was found to increase with the field size at small field sizes and to saturate to a constant value at large field sizes. It reaches amaximum in square fields and decreases as the field becomes elongated. This pattern appears to be quite general: it holds for dispersal kernels that decrease exponentially or faster, as well as for fat-tailed dispersal kernels that decrease slower than exponential (i.e., power-law kernels). We used this approach to estimate R0 in wheat stripe rust(an important disease caused by Puccinia striiformis), where we inferred both the transmission rates and the dispersal kernels from the measurements of disease gradients. For the two largest datasets, we estimated R0 of P. striiformis in the limit of large fields to be of the order of 30. We found that the spatial extent over which R0 changes strongly is quite fine-scaled (about 30 m of the linear extension of the field). Our results indicate that in order to optimize the spatial scale of deployment of fungicides or host resistances, the adjustments should be made at a fine spatial scale. We also demonstrated how the knowledge of the spatial dependence of R0 can improve recommendations with regard to fungicide treatment.

Reduced Virulence of Azoxystrobin-Resistant Zymoseptoria tritici Populations in Greenhouse Assays.

The development of resistance to multiple fungicide classes is currently limiting disease management options for many pathogens, while the discovery of new fungicide classes may become less frequent. In light of this, more research is needed to quantify virulence trade-offs of fungicide resistance in order to more fully understand the implications of fungicide resistance on pathogen fitness. The purpose of this study was to measure the virulence of azoxystrobin-resistant and -sensitive Zymoseptoria tritici populations collected from North and South Willamette Valley, Oregon, in 2012 and 2015. Inoculum mixtures of known fungicide-resistant phenotypes were used to simulate natural field conditions, where multiple genotypes exist and interact in close proximity. Six greenhouse inoculations were conducted over 2 years, and virulence of the isolate mixtures was evaluated in planta. We considered virulence to be "the degree of pathology caused by the organism" and visually estimated the percent area of leaf necrosis as a measure of virulence. In greenhouse conditions, a consistent association of reduced virulence with azoxystrobin-resistant Z. tritici isolate mixtures was observed. North Willamette Valley and South Willamette Valley populations did not differ in virulence.

An Improved Method for Measuring Quantitative Resistance to the Wheat Pathogen Zymoseptoria tritici Using High-Throughput Automated Image Analysis.

Zymoseptoria tritici causes Septoria tritici blotch (STB) on wheat. An improved method of quantifying STB symptoms was developed based on automated analysis of diseased leaf images made using a flatbed scanner. Naturally infected leaves (n = 949) sampled from fungicide-treated field plots comprising 39 wheat cultivars grown in Switzerland and 9 recombinant inbred lines (RIL) grown in Oregon were included in these analyses. Measures of quantitative resistance were percent leaf area covered by lesions, pycnidia size and gray value, and pycnidia density per leaf and lesion. These measures were obtained automatically with a batch-processing macro utilizing the image-processing software ImageJ. All phenotypes in both locations showed a continuous distribution, as expected for a quantitative trait. The trait distributions at both sites were largely overlapping even though the field and host environments were quite different. Cultivars and RILs could be assigned to two or more statistically different groups for each measured phenotype. Traditional visual assessments of field resistance were highly correlated with quantitative resistance measures based on image analysis for the Oregon RILs. These results show that automated image analysis provides a promising tool for assessing quantitative resistance to Z. tritici under field conditions.

How Knowledge of Pathogen Population Biology Informs Management of Septoria Tritici Blotch.

Zymoseptoria tritici (previously Mycosphaerella graminicola) causes Septoria tritici blotch (STB) on wheat. The population biology of Z. tritici has been exceptionally well characterized as a result of intensive studies conducted over nearly 30 years. These studies provided important insights into the biology, epidemiology and evolutionary history of Z. tritici that will prove useful for management of STB. The well-documented, rapid adaptation of Z. tritici populations to fungicide applications and deployment of wheat cultivars carrying both major gene and quantitative resistance reflects the high evolutionary potential predicted by the large effective population size, high degree of gene flow and high levels of recombination found in field populations of Z. tritici globally. QST studies that assessed the global diversity for several important quantitative traits confirmed the adaptive potential of field populations and laid the groundwork for quantitative trait loci (QTL) mapping studies. QTL mapping elucidated the genetic architecture of each trait and led to identification of candidate genes affecting fungicide resistance, thermal adaptation, virulence, and host specialization. The insights that emerged through these analyses of Z. tritici population biology can now be used to generate actionable disease management strategies aimed at sustainably reducing losses due to STB. The high evolutionary potential found in field populations of Z. tritici requires deployment of a corresponding dynamically diverse set of control measures that integrate cultural, chemical, biological and resistance breeding strategies. In this review, we describe and prioritize STB control strategies based on current knowledge of Z. tritici population biology and propose a future research agenda oriented toward long-term STB management.

Evidence of Selection for Fungicide Resistance in Zymoseptoria tritici Populations on Wheat in Western Oregon.

Plant pathogens pose a major challenge to maintaining food security in many parts of the world. Where major plant pathogens are fungal, fungicide resistance can often thwart regional control efforts. Zymoseptoria tritici, causal agent of Septoria tritici blotch, is a major fungal pathogen of wheat that has evolved resistance to chemical control products in four fungicide classes in Europe. Compared with Europe, however, fungicide use has been less and studies of fungicide resistance have been infrequent in North American Z. tritici populations. Here, we confirm first reports of Z. tritici fungicide resistance evolution in western Oregon through analysis of the effects of spray applications of propiconazole and an azoxystrobin + propiconazole mixture during a single growing season. Frequencies of strobilurin-resistant isolates, quantified as proportions of G143A mutants, were significantly higher in azoxystrobin-sprayed plots compared with plots with no azoxystrobin treatment at two different locations and were significantly higher in plots of a moderately resistant cultivar than in plots of a susceptible cultivar. Thus, it appears that western Oregon Z. tritici populations have the potential to evolve levels of strobilurin resistance similar to those observed in Europe. Although the concentration of propiconazole required to reduce pathogen growth by 50% values were numerically greater for isolates collected from plots receiving propiconazole than in control plots, this effect was not significant (P > 0.05).

Multi-location wheat stripe rust QTL analysis: genetic background and epistatic interactions.

KEY MESSAGE: Epistasis and genetic background were important influences on expression of stripe rust resistance in two wheat RIL populations, one with resistance conditioned by two major genes and the other conditioned by several minor QTL. Stripe rust is a foliar disease of wheat (Triticum aestivum L.) caused by the air-borne fungus Puccinia striiformis f. sp. tritici and is present in most regions around the world where commercial wheat is grown. Breeding for durable resistance to stripe rust continues to be a priority, but also is a challenge due to the complexity of interactions among resistance genes and to the wide diversity and continuous evolution of the pathogen races. The goal of this study was to detect chromosomal regions for resistance to stripe rust in two winter wheat populations, 'Tubbs'/'NSA-98-0995' (T/N) and 'Einstein'/'Tubbs' (E/T), evaluated across seven environments and mapped with diversity array technology and simple sequence repeat markers covering polymorphic regions of ≈1480 and 1117 cM, respectively. Analysis of variance for phenotypic data revealed significant (P < 0.01) genotypic differentiation for stripe rust among the recombinant inbred lines. Results for quantitative trait loci/locus (QTL) analysis in the E/T population indicated that two major QTL located in chromosomes 2AS and 6AL, with epistatic interaction between them, were responsible for the main phenotypic response. For the T/N population, eight QTL were identified, with those in chromosomes 2AL and 2BL accounting for the largest percentage of the phenotypic variance.

Identification of Cephalosporium stripe resistance quantitative trait loci in two recombinant inbred line populations of winter wheat.

KEY MESSAGE: Identification of genome regions linked to Cephalosporium stripe resistance across two populations on chromosome 3BS, 4BS, 5AL, C5BL. Results were compared to a similar previous study. Cephalosporium stripe is a vascular wilt disease of winter wheat (Triticum aestivum L.) caused by the soil-borne fungus Cephalosporium gramineum Nisikado & Ikata. In the USA it is known to be a recurring disease when susceptible cultivars are grown in the wheat-growing region of Midwest and Pacific Northwest. There is no complete resistance in commercial wheat cultivars, although the use of moderately resistant cultivars reduces the disease severity and the amount of inoculum in subsequent seasons. The goal of this study was to detect and to compare chromosomal regions for resistance to Cephalosporium stripe in two winter wheat populations. Field inoculation was performed and Cephalosporium stripe severity was visually scored as percent of prematurely ripening heads (whiteheads) per plot. 'Tubbs'/'NSA-98-0995' and 'Einstein'/'Tubbs', each comprising a cross of a resistant and a susceptible cultivar, with population sizes of 271 and 259 F (5:6) recombinant inbred lines, respectively, were genotyped and phenotyped across four environments. In the quantitative trait loci (QTL) analysis, six and nine QTL were found, explaining in total, around 30 and 50 % of the phenotypic variation in 'Tubbs'/'NSA-98-0995' and 'Einstein'/'Tubbs', respectively. The QTL with the largest effect from both 'NSA-98-0995' and 'Einstein' was on chromosome 5AL.1 and linked to marker gwm291. Several QTL with smaller effects were identified in both populations on chromosomes 5AL, 6BS, and 3BS, along with other QTL identified in just one population. These results indicate that resistance to Cephalosporium stripe in both mapping populations was of a quantitative nature.

Degree of host susceptibility in the initial disease outbreak influences subsequent epidemic spread.

Disease epidemics typically begin as an outbreak of a relatively small, spatially explicit population of infected individuals (focus), in which disease prevalence increases and rapidly spreads into the uninfected, at-risk population. Studies of epidemic spread typically address factors influencing disease spread through the at-risk population, but the initial outbreak may strongly influence spread of the subsequent epidemic.We initiated wheat stripe rust Puccinia striiformis f. sp. tritici epidemics to assess the influence of the focus on final disease prevalence when the degree of disease susceptibility differed between the at-risk and focus populations.When the focus/at-risk plantings consisted of partially genetic resistant and susceptible cultivars, final disease prevalence was statistically indistinguishable from epidemics produced by the focus cultivar in monoculture. In these experimental epidemics, disease prevalence was not influenced by the transition into an at-risk population that differed in disease susceptibility. Instead, the focus appeared to exert a dominant influence on the subsequent epidemic.Final disease prevalence was not consistently attributable to either the focus or the at-risk population when focus/at-risk populations were planted in a factorial set-up with a mixture (~28% susceptible and 72% resistant) and susceptible individuals. In these experimental epidemics, spatial heterogeneity in disease susceptibility within the at-risk population appeared to counter the dominant influence of the focus.Cessation of spore production from the focus (through fungicide/glyphosate application) after 1.3 generations of stripe rust spread did not reduce final disease prevalence, indicating that the focus influence on disease spread is established early in the epidemic.Synthesis and applications. Our experiments indicated that outbreak conditions can be highly influential on epidemic spread, even when disease resistance in the at-risk population is greater than that of the focus. Disease control treatments administered shortly after the initial outbreak within the focus may either prevent an epidemic from occurring or reduce its severity.

Durable resistance: a key to sustainable management of pathogens and pests.

This review briefly addresses what has been learned about resistance durability in recent years, as well as the questions that still remain. Molecular analyses of major gene interactions have potential to contribute to both breeding for resistance and improved understanding of virulence impacts on pathogen fitness. Though the molecular basis of quantitative resistance is less clear, substantial evidence has accumulated for the relative simplicity of inheritance. There is increasing evidence for specific interactions with quantitative resistance, though implications of this for durability are still unknown. Mechanisms by which resistance gene pyramids contribute to durability remain elusive, though ideas have been generated for identifying gene combinations that may be more durable. Though cultivar mixtures and related approaches have been used successfully, identifying the diseases and conditions that are most conducive to the use of diversity has been surprisingly difficult, and the selective influence of diversity on pathogen populations is complex. The importance of considering resistance durability in a landscape context has received increasing emphasis and is an important future area of research. Experimental systems are being developed to test resistance gene deployment strategies that previously could be addressed only with logic and observation. The value of molecular markers for identifying and pyramiding major genes is quite clear, but the successful use of quantitative trait loci (QTL) for marker-assisted selection of quantitative resistance will depend greatly on the degree to which the identified QTL are expressed in different genetic backgrounds. Transgenic approaches will likely provide opportunities for control of some recalcitrant pathogens, though issues of durability for transgenes are likely to be no different than other genes for resistance. The need for high quality phenotypic analysis and screening methodologies is a priority, and field-based studies are likely to remain of signal importance in the foreseeable future.