Stripe rust, caused by Puccinia striiformis, has been an important disease of wheat, barley, rye, triticale and certain graminaceous hosts for centuries. The significance of the disease on cultivated cereals has waxed and waned according to the vagaries of climate, inoculum levels and susceptible varieties. A progressive understanding of pathogen biology has revealed levels of specialisation between and within host groups, and these had varying impacts on the hosts concerned. The most economically important form is P. striiformis f. sp. tritici (Pst), the causal pathogen of stripe (yellow) rust of wheat, which is the major focus of this paper. The recent discovery of the perfect stage of Pst on Berberis spp. will encourage further work to uncover the potential importance of the sexual stage in pathogen biology in regions where Berberis spp. occur. A review of the evolution of pathotypes within Pst over the past 50 years reveals recurrent
Stripe rust appears as a mass of yellow to orange urediniospores erupting from pustules arranged in long, narrow stripes on leaves (usually between veins), leaf sheaths, glumes and awns on susceptible plants. Resistant wheat cultivars are characterized by various infection types from no visual symptoms to small hypersensitive flecks to uredinia surrounded by chlorosis or necrosis with restricted urediniospore production. On seedlings, uredinia produced by the infection of a single urediniospore are not confined by leaf veins, but progressively emerge from the infection site in all directions, potentially covering the entire leaf surface. Individual uredinial pustules are oblong, 0.4-0.7 mm in length and 0.1 mm in width. Urediniospores are broadly ellipsoidal to broadly obovoid, (16-)18-30(-32) × (15-)17-27(-28) μm, with a mean of 24.5 × 21.6 μm, yellow to orange in colour, echinulate, and with 6-18 scattered germ pores. Urediniospores can germinate rapidly when free moisture (rain or dew) occurs on leaf surfaces and when the temperatures range is between 7 and 12 °C. At higher temperatures or during the later growing stages of the host, black telia are often produced, which are pulvinate to oblong, 0.2-0.7 mm in length and 0.1 mm in width. The teliospores are predominantly two-celled, dark brown with thick walls, mostly oblong-clavate, (24-)31-56(-65) × (11-)14-25(-29) μm in length and width, and rounded or flattened at the apex.
The wheat stripe rust pathogen (Puccinia striiformis f. sp. tritici; Pst) was first detected in Australia in 1979. The features of the initial pathotype suggested that it was of European origin, and later work provided evidence that it was most likely transmitted as adherent spores on travellers’ clothing. Despite long-held views that this cool temperature pathogen would not adapt to Australian conditions, Pst became endemic and progressively adapted to commercial wheat production through step-wise mutation. Several of these mutant pathotypes became frequent in the Pst population, causing widespread infection and significant costs to production (yield and quality losses; chemical control expenditure) in certain cultivars and seasons. Pathotype evolution, including adaptation to native barley grass (Hordeum spp.) populations, is described. The occurrence of an exotic pathotype of Pst in Western Australia in 2002, and its subsequent spread to eastern Australia, represented a major shift in the pathogen population. This pathotype dominated pathogen populations throughout Australia from 2003, with chemical control expenditure estimated at AU$40–90 million annually. Another exotic introduction was detected in 1998. Initial data indicated that certain isolates collected from barley grass were highly avirulent to wheat differentials, with the exception of partial virulence to Chinese 166. Further seedling tests revealed that these isolates, tentatively designated barley grass stripe rust (BGYR), were virulent on several Australian barleys, notably those of Skiff parentage. Data, including molecular studies, suggest that BGYR is a new forma specialis of P. striiformis. Field nurseries indicate that BGYR is likely to have little impact on commercial barley, although this may change with further pathotype evolution or the release of susceptible cultivars.
Pathogenic attributes of the wheat stripe rust pathogen were monitored in annual surveys from the first recording of this disease in Australia in 1979. During the 10‐year period to 1988,15 different pathotypes were detected in Australia and New Zealand. The pathotypes included some of economic importance to commercial wheat cultivars and others with no obvious selective advantage to aid their survival. Single‐gene mutations were the most likely causes of variation. The implications of these results on pathogenicity surveys and breeding for resistance are discussed.
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