Stripe (yellow) rust, caused by the fungus Puccinia striiformis f. sp. tritici (PST), is a major global wheat disease. New PST strains that show higher infection rates and rapid adaptation to less favourable environmental conditions have been observed over the last 15 years. It has also continued to spread to areas where it was not previously recorded. In South Africa, stripe rust was first detected in 1996. In subsequent years three more PST races were observed, with what seemed to be a step-wise virulence gain. A better understanding of the South African PST pathotypes and how they fit in the global context is needed. We aimed to address this by sequencing the genomes of four historical PST isolates displaying the four distinct virulence profiles. This allowed us to characterise the genetic diversity between these stripe rust races and develop diagnostic markers to easily genotype current detections. We also placed the South African PST isolates in context with global PST isolates where sequence data was available. This analysis illustrates that the South African PST races are more closely related to PST from other African countries when compared to isolates from Africa, Europe and Asia. Through pairwise comparison of isolates, we identified 27 candidate effector genes showing specific polymorphisms between the four isolates that could be related to their distinct virulence profiles. We are currently undertaking gene expression profiling of these candidates to determine if these effectors are specifically upregulated during infection–a key characteristic of effector genes. This study has shed new light on the potential origin and adaptation of stripe rust in South Africa and provides tools for rapid genotypic classification of infections in the field.
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We will present an update on the BBSRC-funded SCPRID project “Maximizing the potential for sustainable and durable resistance to the wheat yellow rust pathogen”. This aims to understand the molecular basis of Puccinia striiformis f. sp. tritici (PST) pathogenicity and exploit this information to design effective breeding strategies that maximize the potential for durable disease resistance in the field. We have established a PST genomics platform through sequencing of PST genomes (UK, European, African, and Indian races) and analysis of expression time courses during infection (Cantu et al 2013). Using this platform we have characterised the PST effector complement, identified putative candidates and have begun their validation. The latest results of this will be presented. We have also evaluated a collection of hexaploid wheat landraces for resistance to PST across continents and have initiated single seed descent mapping populations and initial characterisation in F2:3 populations. We will exemplify the use of new genomic technologies to develop closely linked markers to enable deployment of resistance loci in breeding programmes (Ramirez-Gonzalez et al 2014). We will also provide an update of a new technique, called Field Pathogenomics (Hubbard et al 2015). This method uses transcriptome sequencing of PST-infected wheat leaves to describe pathogen diversity and also identify the host variety. This analysis uncovered a dramatic shift in the PST population in the UK and suggests a recent introduction of a diverse set of exotic PST lineages that may have displaced previous PST populations.
Recent events in worldwide populations of the fungal pathogen Puccinnia striiformis, which causes the yellow rust disease on wheat and other cereals, have suggested that other factors than shifts in virulence can lead to epidemic events. For instance, the spread of two strains across four continents that has occurred within the last 10-15 years seems to be a result of high temperature adaptation combined with a relatively short latent period (Hovmøller et al. 2008; Milus et al. 2009). Variation for quantitative traits like latent period has often been hypothesized to play a significant role in population shift but only very few experimental data have been generated. Here we report difference for components of aggressiveness which included latent period and lesion growth for 17 isolates derived from a selfing of an aggressive isolate using Berberis vulgaris. A group of offspring isolates had a significantly longer latent period and higher lesion growth than the parental isolate. Interestingly, the two traits were found to be positively correlated where a long latent period was correlated with a higher lesion growth rate. This may suggest a trade-off between latent period and lesion growth. All isolates were assessed on seedlings of two highly susceptible host varieties and the two hosts gave similar results. In a previous study the progeny isolates showed segregation for virulence/avirulence and SSR markers (Rodriguez-Algaba et al. 2014). In conclusion, this study demonstrates genetically inheritable variability for latent period and lesion growth in P. striiformis, even within a single parental isolate. The results contribute to a better understanding of the ability of P. striiformis to adapt to new host varieties and changing environments at the quantitative level.
Wheat stripe (Puccinia striiformis f. sp. tritici,=Pst) and stem (Puccinia graminis f. sp. tritici =Pgt) rusts are the most important wheat disease in Egypt as well as present in all wheat growing areas. This study to evaluate a set of tester lines of wheat carrying stripe Yr's, stem Sr's rust genes and selected Egyptian varieties have been studied for their response to Pst and Pgt at adult plant stage under field conditions in Sakha Agriculture Research Station, during the 2011 to 2014 growing seasons. The results revealed that stripe rust, it has been observed that the new race Yr27-virulence to Pst. In addition pathotypes were virulent for Yr2, Yr6, Yr7, Yr8, Yr9, Yr27, while Yr18 showed moderate susceptibility. On the other hand, Yr1, Yr5, Yr10, Yr15, Yr17, Yr32 and YrSP exhibited high levels of resistance. Regarding, evaluation of resistance genes sources of stem rust on ICARDA, CIMMYT wheat germplasm, and Egyptian wheat varieties released i.e. Misr1 and Misr2 which having Ug99_resistance genes Sr2 and Sr25 were found susceptible to Pgt, also Sr31 recorded infection moderately susceptible to susceptible at adult stage. Genes Sr2 complex, Sr24, Sr26, Sr27, and Sr32 were resistant at adult plant stages. The combination of Sr26 with Sr2 and Sr25 provided stem rust resistance in some CIMMYT wheat germplasm. The objectives of this work are: race analysis of wheat stem and stripe rust disease, evaluation the level and distribution of wheat stripe and stem rust in Egypt, and identification the resistance genes in commercial varieties or new promising lines using standard and molecular genetic markers. Egyptian germplasm such as Misr1, and Misr2 and others tester lines of wheat carrying stem rust Sr's were evaluative under field condition at adult stage in Egypt during 2014 growing season, Egyptian cultivars Misr1 and Misr2 were susceptible rated 10S-20S and Sr31 rated MSS. that results clearly presence a new Sr31-virulence. On other hand, genes Sr2 complex, Sr24, Sr26, Sr27 and Sr32 were resistant and combination of Sr26 with (Sr2 and Sr25) produced stem rust resistance in some CIMMYT wheat germplasm. Shahin et al., 2015, in APS Annual Meeting, Aug. 1-5, Pasadena, CA, US, (In Press).
Stripe rust is one of the major diseases of wheat worldwide. The causative fungus, Puccinia striiformis f.sp. tritici (Pst), keeps the infected tissue alive even after sporulation phase, a strategy that is referred to as biotrophy. The compatible interaction is divided into three phases; colonization, growth, and sporulation, the last occurring ~14 days after germination of spores. During the growth phase plant apoplast is completely occupied by hyphae, and the fungus develops special invasive structures called haustoria within plant cell. Both hyphae and haustoria are thought to take up nutrients from the host, but haustoria are specialized for this role. However, it is still unknown how the fungus obtains nutrients; perhaps by direct manipulation of host metabolic pathways related to photosynthesis or by changes in whole plant metabolite fluxes by acting as a sink. Also, it is unclear why wheat plants do not detect either the fungus itself, or the consequent loss of nutrients. The aim of this study is to understand the changes during the three phases of infection, comparing metabolites and plant photosynthetic efficiency in healthy and infected tissue, and correlating this with fungal growth. The results show that CO2 assimilation rates decreased only at the sporulation phase, which correlates with a reduction in transitory starch accumulation. However, glucose and fructose levels were lower only during colonization phase. Interestingly, although the infection alters the nutrient balance, this did not seem to affect the development of young leaves. In addition to these results, we found that stripe rust grows faster in younger leaves, which might be related to their morphology and the nutrient availability and fluxes within the leaf. This research suggests that the fungus is undetected until sporulation, and will aid future studies to understand the mechanisms of adult plant resistance conferred by transporter proteins. The research will aid future studies to understand the dynamic of adult plant resistance conferred by transporter proteins. The knowledge in wheat physiology and metabolism during rust infection could help to explain the role of transporter proteins during wheat-stripe interaction in different plant growth stages.
The Himalayan region of Pakistan has been shown to be the centre of diversity of wheat yellow rust pathogen Puccinia striiformis f.sp. tritici (Pst) with a probable role of sexual reproduction in the population temporal maintenance. However, the populations of southern part of Pakistani Himalayan region remains unexplored, where wheat yellow rust is an important disease on rainfed wheat. The current study was thus carried out to assess the disease status and population structure of Pst prevalent in the southern part of Pakistani Himalayan region, mainly the districts of Kohat, Karak, Bannu, Lakki-Marwat and DI-Khan. A high disease pressure was observed during wheat season in 2013 in the region, where the level of severity ranged from 5% to 100% depending upon the variety tested. Microsatellite genotyping of 102 isolates with 18 SSR markers revealed a high diversity ranging from 0.86 (for DI Khan) to 1.00 (for Karak). The recombination signature was lower compared to the Himalayan populations. Analyses of the population subdivision revealed no clear evidence of spatial structure, with the maximum FST value of only 0.081. The overall diversity was higher in the region as compared to European clonal population, though it was still lower than the recombinant Himalayan populations, which could be attributed to their distance from Berberis spp. plantation zone.
This is the first study on the inheritance and genetic mapping of resistance to the barley grass stripe rust pathogen (Puccinia striiformis f. sp. pseudohordei – Psph) in bread wheat. Psph, commonly infects barley grass (Hordeum leporinum, H. murinum), but about 10% of commercial barley varieties are also susceptible. We tested over 500 diverse wheat accessions and determined that less than 20% were susceptible at the seedling stage suggesting wheat is an ‘intermediate’ host to Psph. The Australian variety Teal is highly susceptible to Psph at the seedling stage, whereas selections Avocet S and Avocet R are highly resistant and resistant, respectively. We used the Teal/AvocetR doubled haploid (DH) population to characterize the resistance of Avocet R to Psph and determine whether the complementary genes Yr73 and Yr74 (YrA resistance) in Avocet R conferred resistance to Psph. Phenotypic comparison of the Teal/AvocetR DH lines in response to both Psph and Pst showed that all DH lines carrying YrA were also resistant to Psph; however, fewer DH lines were susceptible to Psph suggesting additional resistance genes. Marker-trait association analysis detected three DArT-Seq markers significantly associated with resistance to Psph, two mapping to chromosomes 3DL and 5BL in the same regions as Yr73 and Yr74 and the third mapping to chromosome 4A. Single gene stocks with the 4A gene and combinations of the 5BL and 3DL genes will be used for monitoring avirulence/virulence within Australian Psph population. Genetic analysis of seedling-susceptible T/AvR DH lines as adult plants in the greenhouse determined that Teal and Avocet R each carried at least one APR gene effective against Psph.
There is emerging evidence that the geographical footprint of stripe rust is expanding, opening up prospects for an increase in economic losses attributable to this disease worldwide. Drawing on newly compiled data, along with insights obtained from a survey initiated at the BGRI meeting in New Delhi in August 2013, this talk will report on efforts to model the global occurrence and persistence of stripe rust in a geo-spatially sensitive fashion. Using the available data in conjunction with these newly developed climate suitability maps, I will present probabilistic crop production losses associated with the disease and place an economic value on the prospective losses. Given changes in the geographical spread of this disease, and the associated uncertainties about its likely wheat yield and economic effects, various scenarios will be assessed to inform and thereby help shape the research investment decisions regarding crop breeding and other options for ameliorating these prospective losses over the longer term.
In 2010, Ethiopia experienced one of the largest stripe rust epidemics in recent history. Over 600,000 ha of wheat were affected, an estimated 60 million Ethiopian Birr ($US3.2 million) were spent on fungicides and large production losses were observed. Factors associated with the 2010 epidemic were conducive climatic conditions (prolonged rain and apparently optimal temperatures), large areas planted to susceptible cultivars, early infection and rapid spread of a virulent pathogen, a low level of awareness, and ineffective control measures. In 2013, highly favourable climatic conditions and early appearance of stripe rust showed remarkable similarity to the conditions observed in 2010, prompting fears of a similar major rust epidemic. However, no stripe rust epidemic developed in 2013. In contrast, only limited and localized outbreaks of stripe rust were observed in 2013; wheat crops remained in good condition and a good harvest was achieved. It seems that a series of positive and timely actions in Ethiopia contributed to the markedly different stripe rust situation in 2013 compared to 2010. The principle factors associated with the positive outcomes in 2013 are (i) effective promotion, plus rapid and widespread adoption of rust resistant wheat cultivars since 2010 - this dramatically reduced the vulnerability of the Ethiopian wheat crop; and (ii) timely and coordinated surveillance efforts, coupled to good information exchange amongst different stakeholders - this resulted in effective control and awareness campaigns that targeted emerging stripe rust outbreaks. A comparative analysis is presented which highlights the similarities and disparities between the 2010 and 2013 stripe rust situations in Ethiopia. The roles and contributions of different organisations are examined and an in-depth analysis of the biophysical conditions in the different years is presented.
A number of rusts affect grain crops in Sweden, but stem rust on oats and stripe (yellow) rust on wheat appear to create the greatest problems in production. The epidemiology of these diseases is intimately connected to the overall cropping patterns of these two crops. In Sweden, oats are only sown in the spring, thus forcing any overwintering pathogen to survive a Swedish winter. This is easiest for Puccinia graminis f. sp. avenae, which apparently completes its full, sexual life cycle on the abundant barberry plants. The presence of barberry and clear indications of sexual reproduction by P. graminis suggests that Pgt could be a problem on wheat, but there are only sporadic reports of stem rust on wheat. Wheat cultivars grown in Sweden possess few effective genes for resistance to stem rust, and the lack of rust is probably due to a lack of Pgt in the region. Given the resurgence of barberry in the landscape this implies that stem rust on wheat could be a major problem if (or when) the pathogen returns. P. striiformis, in contrast, can survive the Swedish winters on fall sown cereal crops, and thus it is the fittest clones that survive and dominate in the population. A large number of factors can affect this fitness, most markedly resistance genes in the cultivated wheat, but it is also possible that extended asexual reproduction can reduce the fitness of these persistent clones (Muller's ratchet) so that they can be displaced by fitter clones. Despite the widespread occurrence of barberry plants, we have not found any aecia of P. striiformis, although there does seem to be some genetic variation in the alternate host. Simple models that simulate the appearance and competition between different clonal lineages of the pathogen indicate that fitter individuals will eventually dominate the population, but their initial appearance will be difficult, since they are only detectable after enough generations have passed to increase the population size above a detectable level.