Abstract
Two techniques (mobile seedling nursery and detached leaf) were used to study the pathogenic variability of Erysiphe gramznis DC. ex Merat f.sp. hordei Em. Marchal in four barley growing areas of South Australia (S.A.). The mobile nurseries were conducted over 5 years (1981-1985) to monitor changes in the spectrum of virulence and individual gene frequencies. The race-specific resistance genes M1-a6, M1-k, M1-v and M1-ra were found to be susceptible to the pathogen populations in all surveyed areas. The same virulence genes spectrum (V-a6, V-k, V-v and V-ra) was present in the pathogen populations in the surveyed areas throughout the period of 1981-1984. During the 1985 season, one new virulence matching the resistance gene in cv. Forrest was detected. The resistance in cv. Galleon did not 'break down' over the cultivation period when its cultivation rose to 55% of the barley areas of S.A. The probable reasons for apparent durability of Galleon resistance are discussed. The relative frequencies of the matching virulence genes varied only slightly over time and space. The relative frequency of V-k was always almost 100%. The relative frequencies of V-a6, V-ra and V-v occurred at a higher rate than expected, since the matching resistance genes were not deployed in barley cultivars. The results of the detached leaf experiments (1982-1984) confirmed the virulence spectrum of the pathogen populations found in the mobile nursery experiments. Three individual single colony isolates from different cultivars (Clipper, Sonja and Goldmarker) were isolated and purified. Each isolate can produce a susceptible infection on other cultivars having different resistance genes in addition to its matching cultivar. Thus, each isolate carries more than one virulence gene. In the mobile nursery tests, the resistance gene M1-v (Varunda and LaMi) showed variable infection types (I.T.l-3), but in most cases it was moderately susceptible (I.T.3). Under the controlled conditions of the detached leaf tests, it gave an I.T.3 indicating the presence of virulence gene for M1-v in the pathogen populations. Reasons for this variable reaction are discussed. Midas with an ineffective gene (M1-a6) produced a resistant reaction to all isolates, suggesting the presence of additional resistance genes in the cultivar. The Mildew resistance genes M1-a, M1-a7, M1-a9, 141-al2, M1-g, M1-h, M1-(CP) and ml-o3 were found to be resistant in all surveyed areas in both experiments throughout S.A. Either the matching virulence genes for these resistance genes were absent or they were present at a very low frequency in the pathogen populations that could not be detected by the sampling techniques used.
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