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The importance of monitoring and management of yellow rust, caused by Puccinia striiformis f. sp. tritici (Pst), has markedly increased in Russia over recent years because of intensifying negative effects of this destructive disease on wheat production. The Pst virulence survey was conducted in 2019–2021 in the European (North‐West, Volga, North Caucasus) and Asian (Siberia) parts of Russia, and the same 109 isolates have been genotyped here with 20 SSR markers. Fifty‐three multilocus genotypes (MLGs) were detected, seven of which occurred in two or more regions. The most frequent MLG was found in three European Pst collections (except Dagestan) and Siberia. SSR‐based variation within the regional collections was low because many MLGs were closely related. Nevertheless, each collection contained relatively different small genotype groups. No clear geographic structure of the Russian Pst population was observed because the five studied regional collections shared groups of similar genotypes. The most singular SSR genotype was identified in the North‐West collection, but genotypes of four invasive isolates belonging to the PstS2 temperature‐adapted aggressive strain did not considerably differ from others. The observed heterozygosity at all SSR loci exceeded the expected one in all regional Pst collections, which could imply asexual reproduction of the pathogen. Both the SSR and virulence analyses demonstrated similar patterns of relationships between the regional Pst collections, although the magnitude of differences between the collections was larger for virulence pathotypes. However, no significant association was established between the virulence pathotypes and SSR genotypes because multiple pathotypes had the same genotype and vice versa. [ABSTRACT FROM AUTHOR]

Wheat stripe mosaic virus (WhSMV) is the causal agent of soilborne wheat mosaic disease (SBWMD) in Brazil, which is a serious threat to wheat production in the southern part of the country. WhSMV also occurs in Paraguay and South Africa. The virus is soilborne, transmitted by Polymyxa graminis, and management strategies are mainly based on genetic resistance. Variation in the reaction (type and severity of symptoms) of cultivars has been reported depending on the region and/or year of cultivation, leading wheat breeding programmes to test their materials in several locations, which increases costs and is time‐consuming. One hypothesis is that this variation in symptoms is a result of the genetic variability of WhSMV. We assessed the genetic variability and population structure of WhSMV infecting wheat in Brazil and South Africa. In field experiments conducted in different locations in southern Brazil, a consistent reproducibility of symptoms was observed in a set of cultivars, and molecular analysis showed a low degree of genetic variability of the Brazilian viral population. The hypothesis that the variation in SBWMD symptoms in Brazil is due to genetic variability of the virus was thus rejected. Comparison of the Brazilian and South African WhSMV isolates indicated that they comprise distinct subpopulations and that the Brazilian subpopulation is more variable than the South African subpopulation. The lower genetic variability of the South African subpopulation suggests genetic stability or a recent emergence of WhSMV in that region. [ABSTRACT FROM AUTHOR]

The worldwide spread of wheat yellow rust lineage PstS1/S2 adapted to higher temperatures prompted us to investigate how diverse temperature responses of this lineage are in the Middle East, where diversity was previously observed within this lineage for pathotypes and genotypes. Here we highlight the diversity of response to temperature within a PstS1/S2 population. Twenty‐six isolates from eight countries and different altitudes, which were tested under four combinations of cold and warm incubation and postincubation temperature conditions, showed diversity for infection efficiency (IE) and latency period (LP). IE of the various isolates ranged from 5.8% to 13.7% under cold (5°C) and 0.04% to 1% under warm (20°C) incubation temperatures. LP varied from 10.2 days under warm to 4.43 days under cold incubation. LP of isolates from the same country could differ by 2 days. Significant differences in thermal aptitudes of the isolates were observed between and within countries. IE and LP diversity was not related to altitude origin of the isolates on the whole; however, a trade‐off between IE and LP was observed for isolates from low altitude (<400 m) under a warm regime. We showed diversity for thermal aptitude for IE and LP of isolates belonging to the same PstS1/S2 lineage. Understanding Pst temperature aptitude among geographically distant isolates of the same clonal lineage may help to identify the geographic range of pathogens and also to improve forecast models or breeding programmes. [ABSTRACT FROM AUTHOR]

The expression of the resistance phenotypes of QPst.jic-2D and QPst.jic-4B, two quantitative trait loci (QTL) for stripe rust resistance in wheat cv. Alcedo, were assessed relative to plant growth stage, while a histopathology analysis was undertaken to characterize the cellular interaction between Puccinia striiformis f. sp. tritici (the causal agent of stripe rust) and each QTL. QPst.jic-2D expressed a partial resistant phenotype at seedling growth stages, with the level of resistance increasing as the wheat plant matured, conferring a disease-free phenotype at heading. QPst.jic-4B, however, did not express a resistant phenotype until booting (growth stage 41 on the Zadoks scale), displaying its full resistant phenotype at heading. Microscopic examination in flag leaves showed that infection sites formed in all genotypes tested, with full infection-site establishment being observed by 36 h post-inoculation (hpi). In lines carrying both QPst.jic-2D and QPst.jic-4B, as well as the parental cv. Alcedo, no microcolony formation, defined by the appearance of runner hyphae, was observed. Microcolony formation was observed in lines carrying only one, or neither QTL. Cell death associated with infection sites was observed for all genotypes, although the timing of first appearance and the extent of the cell death response varied considerably. In lines carrying both QPst.jic-2D and QPst.jic-4B cell death did not extend beyond one to three cells. In lines carrying only one QTL more extensive cell death was observed and cell death appeared later in lines with QPst.jic-4B than QPst.jic-2D. Cell death was also occasionally observed in lines without either QTL, although only at 264 hpi. [ABSTRACT FROM AUTHOR]

The size and shape of field plots can impact on both the cost and outcome of epidemiological experiments. In previous studies, epidemic velocity of yellow rust (caused by Puccinia striiformis f.sp. tritici) on wheat ( Triticum aestivum) has been examined in long, narrow plots (6·1 m by 73–171 m). The present study compares spread in square, 61 × 61 m plots versus narrow, 6·1 × 61 m plots at two locations. The objective was to test whether plot shape has a substantial impact on spatiotemporal spread of yellow rust. Velocity increased curvilinearly with time for both plot shapes and at both locations. Curves of epidemic velocity versus time were nearly identical in square versus narrow plots in both the upwind and downwind directions. Contrary to expectation based on simulations, the results did not indicate faster disease spread in square plots, though the plot sizes studied may be beyond that at which there is a rapid change of disease increase with increasing plot area. Velocity also increased curvilinearly in all eight compass directions of the square plots. Results indicate that narrow plots, which are substantially less costly than equidimensional plots, may be justified for studying the spatiotemporal spread of wheat yellow rust and other diseases with similar epidemiological characteristics. [ABSTRACT FROM AUTHOR]

A series of experiments was conducted with wheat stripe rust to analyse competition between simple and complex pathotypes in host mixtures. Two different pathotype combinations were tested, with different host components. Each combination included a complex (able to infect two host components) and two simple pathotypes. For one of the combinations, induced resistance was tested in a separate experiment as a possible interaction among pathotypes. Disease severity and pathotype frequencies were measured three times during the epidemic, on each host component grown in pure stands and in mixtures. In one of the experiments, pathotype frequencies were also measured within secondary foci. One of the complex pathotypes appeared to have a low fitness on one of the host components and did not significantly increase in frequency in host mixtures relative to pure stands. The average frequency of the other complex pathotype increased during the first epidemic cycles, but remained stable afterwards, below expected values. The results suggest that the development of complex pathotypes in host mixtures may be influenced by differential aggressiveness on the host components, by induced resistance and by random effects resulting from the formation of disease foci, and depends on pathogen autoinfection rate and dispersal mechanisms. [ABSTRACT FROM AUTHOR]