Effects of Resistance Gene Deployment on Pathogen Populations

Disease control strategies in barley, particularly against powdery mildews and rusts, are continually eroded in their effectiveness as the pathogen adapts to overcome them. This includes both application of crop protectants and 'ecological' approaches such as the use of cultivar mixtures, which select more complex powdery mildew races than the component monocultures. Knowledge of the mildew population structure and how it changes in response to control measures will help to devise strategies for minimising pathogen adaptation.Morphological variation amongst single-spore derivatives from a Stagonospora (Septoria) nodorum isolate

The success of mixtures of cultivars expressing major genes for resistance is dependent on a pathogen population where a substantial proportion does not express virulence matching all the host resistance genes. Even then, mixtures will tend to select for complex isolates which overcome all the resistance genes. If the population comprises few genotypes or only simple genotypes, then, provided these do not include virulence towards all the resistance components in the mixture, disease reduction is likely to be highly effective. However, if the population is highly heterogeneous and complex isolates occur, a little disease reduction may occur early in the epidemic but is likely to be eroded as complex pathotypes virulent on all components, are selected.

Disease control based on the use of resistance elicitors, which are being developed by several agrochemical companies and research groups including ourselves at SCRI may be less prone to erosion by pathogen population selection. This is because they act by triggering the plants defence mechanisms enabling them to express resistance better upon actual challenge by a pathogen. It is assumed that they act non-specifically against all pathotypes, but it is also known that they cause differential expression of resistance in different cultivars of barley.

We study pathogen populations to determine both the mechanisms of adaptation [2, 4, 5, 6, 8, 12, 14, ], and changes that occur in the field in practice [1, 3, 7, 9, 10, 11, 13, 15, 16].

Refereed publications

[1] Newton AC, Caten CE Johnson R, 1985. Variation for isozymes and double-stranded RNA among isolates of Puccinia striiformis and two other cereal rusts. Plant Pathology 34, 235-247.

[2] Newton AC, Johnson R Caten CE, 1986. Attempted somatic hybridisation of Puccinia striiformis f.sp. tritici and P.striiformis f.sp. hordei. Plant Pathology 35, 108-113.

[3] Newton AC, 1987 Occurrence of double-stranded RNA and virus-like particles in Septoria nodorum. Transactions of the British Mycological Society 88,113-116.

[4] Newton AC, Caten CE, 1988. Auxotrophic mutants of Septoria nodorum isolated by direct screening and by selection for resistance to chlorate. Transactions of the British Mycological Society 90, 199-207.

[5] Newton AC, 1988. Mutant instability in Septoria nodorum. Transactions of the British Mycological Society 91, 607-610.

[6] Newton AC, 1988. Somatic recombination in Rhynchosporium secalis. Plant Pathology 38, 71-74.

[7] Newton AC, 1989. Genetic adaptation of Erysiphe graminis f.sp. hordei to barley with partial resistance. Journal of Phytopathology 126, 133-148.

[8] Newton AC, 1990. Isozyme variability in isolates of some facultative phytopathogenic fungi. Journal of Phytopathology 131, 199-204.

[9] Newton AC, McGurk L, 1991. Recurrent selection for adaptation to partial resistance in barley by Erysiphe graminis f.sp. hordei. Journal of Phytopathology 132, 328-338.

[10] Newton AC, Caten CE, 1991. Characteristics of strains of Septoria nodorum adapted to wheat and to barley. Plant Pathology 40, 546-553.

[11] Newton AC, 1992. Selection for aggressiveness towards partial resistance in barley by Erysiphe graminis f.sp. hordei. Journal of Phytopathology 136,165-169.

[12] Rohe M, Searle J, Newton AC, Knogge W, 1996. Transformation of the plant pathogenic fungus Rhynchosporium secalis. Current Genetics 29, 587-590.

[13] Jennings JM, Newton AC, Buck KW, 1997. Detection of polymorphism in Puccinia hordei using RFLP, RAPD and differential cultivars and analysis of the intergenic spacer region of rDNA. Journal of Phytopathology 145, 511-519.

[14] Newton AC, Osbourn AE, Caten CE, 1994. Heterokaryosis and vegetative incompatibility in Stagonospora nodorum. Mycologia 90, 215-225.

[15] Newton AC, Hackett CA, Guy DC, 1998. Diversity and complexity of Erysiphe graminis f.sp. hordei collected from barley cultivar mixtures or barley plots treated with a resistance elicitor. European Journal of Plant Pathology 104, 925-931.

[16] Caten CE, Newton AC, 2000.Variation in cultural characteristics, pathogenicity, vegetative compatibility and electrophoretic karyotype within field populations of Stagonospora nodorum. Plant Pathology 49, (in press).

Non-refereed publications

[17] Newton AC, 1987. Markers in pathogen populations. In: Genetics and Plant Pathogenesis. (ed. P.R. Day G.J. Jellis), pp.187-194. Blackwells Scientific Publications, Oxford.

[18] Newton AC, Caten CE, 1985. Heterokaryosis and heterokaryon incompatibility in Septoria nodorum. In: Septoria of cereals (ed. A.L. Scharen), pp.13-15.United States Department of Agriculture, ARS-12.

[19] Newton AC, Johnson R Caten CE, 1985. Virulence analysis of local populations of Puccinia striiformis f.sp. tritici. Cereal Rusts Bulletin 13, 11-15.

[20] Newton AC, 1986. The function of mycoviruses in cereal rusts. Cereal Rusts Bulletin 15, 58-60.

[21] Newton AC, 1991. Understanding and interpreting isozyme variability in fungi. Cereal Rusts and Powdery Mildews Bulletin 18, 61-66.

[22] Smith JM, Buck KW, Newton AC, 1991. DNA polymorphisms as genetic markers for the cereal rust fungi. Abstr. Genetics Conference, USA.