The development of cultivars resistant to cereal cyst nematode (CCN) is a primary objective in wheat breeding in the southern wheatbelt of Australia. Nine CCN resistance genes have been identified in wheat and its relatives, some of which confer resistance to the Australian pathotype of CCN (Ha13). Cultivars released in Australia with CCN resistance carry either the Cre1 or CreF gene, with the Cre3 gene present in advanced breeding lines. The biological assay for CCN resistance screening in wheat is time-consuming, not reliable on a single-plant basis, and prone to inconsistencies, thus reducing the efficiency of selection amongst breeding lines. Using gene sequences initially isolated from the Cre3 locus, a DNA-based marker selection system was developed and applied to unambiguously identify wheat lines carrying resistance alleles at theCre1 and/or Cre3 loci in breeding populations derived from diverse genetic backgrounds. Homologues of sequences from the Cre3 locus, located elsewhere in the wheat genome, can also be used to select wheat lines with a newly identified CCN resistance gene (Cre6) introgressed from Aegilops ventricosa. Application of these markers has become an integral part of the southern Australian breeding programs.
A model describing the population trends for any number of races of rust in the urediospore stage during a single growing season is presented. The general case for the field is subsequently modified to describe trends in a population of rust races under constant conditions. A term which gives an estimate of the relative survival ability of each race in the population is finally obtained. This term allows the trends in the composition of the mixture to be predicted. The theoretical proportion of strain 21 Anz-2,3,7 in amixture of strains 21 Anz-2,7 and 21 Anz-2,3,7 of P. graminis trifici over a number of generations was compared with the proportion of strain 21 Anz-2,3,7 in an experimental population of the same two strains over the same period. The model was found to be a good first approximation to the results obtained with the experimental population.
The effect of A. helianthi on yield of sunflower (cv. Hysun 30) was assessed in two field trials at Hermitage and Gatton in southern Queensland during the 1977-78 season. Plots were (i) inoculated with spore suspensions of A. helianthi to encourage an epidemic or, (ii) sprayed regularly with the fungicide captafol to prevent disease development. Conditions were dry at both trial sites except for one week of wet overcast weather when an epidemic of A. helianthi developed. At this time, plants in the Hermitage trial were commencing anthesis, while those in the Gatton trial were approaching maturity (4 weeks post anthesis). After the wet period the epidemic declined in the Hermitage trial, and a low level of disease was present at maturity. At Gatton the disease caused premature leaf senescence in unsprayed plots, while foliage in sprayed plots remained green. Control of the epidemic that began at anthesis increased oil yield by 28%, mainly through increased seed number. There was also a small increase in 1000 seed weight but no significant increase in oil content. Control of the epidemic that began just before maturity increased oil yield by 20%, mainly because of increased 1000 seed weight and a small increase in oil content. It appears that the plant growth stage at the time the disease epidemic occurred determined which yield attributes were most affected.
Oil yield losses in sunflower (cv. Peredovic) caused by rust infection (Puccinia helianthi) were greatly influenced by the growth stage of the plant when infection occurred and by the intensity of infection. Simulated epidemics produced under greenhouse conditions, where plants were first inoculated at the vegetative, budding, anthesis or seed development stages of growth and thereafter at 10 day intervals, resulted in reductions in oil yield of 85, 73, 38 and 13% respectively relative to those in uninoculated controls. In contrast, plants inoculated once only at each of these growth stages showed reductions in 011 yield of 13, 42, 35 and 10% respectively. When plants were inoculated at the vegetative stage and thereafter at 10, 20 and 40 day intervals, the reductions in oil yield were 85, 79 and 64% respectively relative to uninoculated controls. The reduction in oil yield of infected plants was caused by a reduction in the number of seeds produced per head, the weight of individual seeds and the percentage oil content of seeds. The effects of rust infection on other parameters showed similar trends to that on oil yield.
Sunflower rust intensity in crops of several hybrid cultivars in Queensland during the 1980, 1981 and 1982 seasons ranged from 30 to 60% of leaf area. In previous years, these cultivars had rust ratings of 2-5%. Rust was also found on some crops of usually immune hybrids grown during winter in central Queensland. A number of rust differential lines were inoculated with several isolates collected from throughout Queensland during 1981 and 1982, as well as with isolates stored in liquid nitrogen from the years 1976, 1978 and 1980. Because all isolates failed to infect the differentials possessing either the R1 or R2 genes for resistance, all collections were allocated to race 1. Comparisons of the temporal isolates revealed that no differences could be detected among the generation times, pustule number and pustule size produced by isolates on a range of sunflower rust differentials and hybrid cultivars. These data indicated that the composition of the pathogenic population had not altered. The application of higher inoculum densities shortened generation times and produced more pustules; both relationships were linear. The development of race 1 rust on seedlings of the immune hybrid Hysun 30 was induced by maintaining the plants under low light intensity or short photoperiods.
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