
%0 Journal Article
%A Vinijsanun, T 
%A Cameron, DF 
%A Irwin, JAG 
%A Barnes, A 
%T Phenotypic variation for disease resistance and virulence within naturalized populations of <I>Stylosanthes humilis</I> and <I>Colletotrichum gloeosporioides</I>
%J Australian Journal of Agricultural Research
%D 1987/08/01
%V 38
%N 4
%P 717-728
%K 
%R https://doi.org/10.1071/AR9870717
%U https://www.publish.csiro.au/paper/AR9870717 
%X The extent of variation for host disease reaction and pathogen virulence was studied in naturalized populations of Stylosanthes hurnilis and Colletotrichurn gloeosporioides, the causal fungus of an anthracnose disease of Stylosanthes spp. Diseased plants (S0) were collected from the field at three sites (Townsville, Wrotham Park and Niall) in North Queensland, and first generation selfed (S1) progenies (host-lines) and single spore fungal cultures were grown for each of the collections made. Within a site, all host-lines were inoculated with each fungal isolate from that site, and a fourth experiment was conducted with representative host-pathogen combinations from each site. Sufficient seed was obtained to allow testing of 12, 10 and 8 collections from Niall, Wrotham Park and Townsville respectively. Significant variation (P < 0.01) between disease severity values for host-line means, fungal isolate means and host-line/fungal isolate interactions was found in all four experiments. Differences between fungal isolate means were the main source of variation in three of the four experiments. Both the differences in virulence within the pathogen population and the differences in resistance of the hostlines appeared to be quantitatively inherited. One host-line from Wrotham Park was significantly more resistant than the susceptible check, cv. Paterson, in two replicated experiments indicating that selection for some improvement in resistance within the naturalized populations should be possible. However, none of the host-lines from the Townsville and Niall sites were significantly more resistant than Paterson, suggesting that little natural selection for resistance has occurred within the naturalized host populations over the 10 years following the first outbreak of the disease in northern Australia. 
