A range of inocululatron methods for assessing resistance in wheat to crown rot caused by Fusarium graminearum Group 1 was evaluated in the glasshouse and in the field. When grain was colonized with the pathogen, ground and applied with the seed at planting or spread around young plants as an aqueous suspension, high levels of crown rot were produced, but resistance (usually measured as per cent diseased plants or tillers) was still expressed. Similar results were achieved with induced field inoculum obtained by inoculating an area of wheat to obtain a high incidence of disease and incorporating the stubble into the soil. Natural field inoculum and inoculation of seed with spores produced lower levels of disease, although differentiation of resistant and susceptible cultivars was still possible. Other methods, suitable only for plants in pots and often for more specific purposes (for example, for inoculation at different stages of plant growth) were also studied. Resistance was best expressed where inoculum was applied onto or into soil, rather than directly onto or into plants. Currently, the resistance of all potential cultivars for release in Queensland is assessed in the field by sowing seed dusted with benomyl into furrows along which ground, colonized grain is distributed. Crown rot severity is then determined at maturity.

Australian isolates of Fusarium pseudograminearum (Fp = F. graminearum Group 1) and F. graminearum (Fg = F. graminearum Group 2) can produce mycotoxins including zearalenone (ZEA), 4-deoxynivalenol (DON), and nivalenol (NIV). Fp isolates from wheat and barley tillers in southern Queensland all produced ZEA and DON in culture, and one typical isolate also produced 3-acetyldeoxynivalenol. Most Fg isolates from wheat and sorghum grains in southern Queensland produced ZEA and DON and one typical isolate also produced 15-acetyldeoxynivalenol. Fg isolates from maize plants in northern Queensland were all ZEA and NIV producers, which was consistent with previous reports, and they also produced high concentrations of acetyl-nivalenols. ZEA and either DON or NIV production by cultures derived from different conidia (and ascospores in Fg isolates) varied by 4-18-fold for ZEA and 2-4-fold for DON/NIV production, and there were significant negative correlations between ZEA and either DON or NIV, indicating a common controlling process. The pattern of ZEA production was quite different between Fp and Fg, with ZEA production being relatively delayed in Fg. After 7 days incubation at 28°C on maize meal, one Fp isolate produced 49 mg ZEA/kg, but in both DON-producing and NIV-producing isolates of Fg, ZEA concentrations after 7 days were <1 mg/kg. ZEA and DON were produced on sorghum and combined wheat-barley grains as well as maize meal, although there were trends for maize meal to be more productive, probably due to greater surface area or different gaseous exchange. Low temperature incubation of a Fg DON-type isolate increased ZEA production, but did not affect either a Fg NIV-type isolate or a Fp isolate. Relationships between these patterns of mycotoxin production, pathogenicity, and implications for crop contamination are discussed.

The production of the mycotoxins zearalenone (ZEA), 4-deoxynivalenol (DON) and nivalenol (NIV) by isolates of Fusarium graminearum from different crops and regions in Queensland was examined in maize meal incubated for 28 days at 28�C. Sixteen isolates of F. grarninearum Group 1 from wheat and barley stalks and a wheat seed in southern Queensland produced ZEA (range 208-2367, median 833 mg kg-1) and DON (range 3-28, median 15 mg Kg-1). One Group 1 isolate from a wheat stalk was unlike these 16, producing 2 mg ZEA kg-1 and 168 mg DON kg-1. Fifteen isolates of F. graminearum Group 2 from wheat seeds and spikelets, and sorghum and maize stalks in southern Queensland produced ZEA (range 25-2280, median 629 mg kg-1) and DON (range 11-904, median 200 mg kg-1. Three isolates from wheat seeds produced ZEA (range 5-41, median 15 mg kg-1) and NIV (range 10-75, median 40 mg kg-1). All 23 isolates of F. graminearum Group 2 from maize seeds and stalks in northern Queensland produced ZEA (range 3-228, median 40 mg kg-1) and NIV (range 8-270, median 26 mg kg-1). Group 1 isolates tended to produce more ZEA and less DON than Group 2 DON-producers, but there was a degree of overlap. Group 2 NIV-producers generally produced less ZEA than Group 1 and Group 2 DON-producers. No relationship between either climate or host and mycotoxin production was detected.

Evidence is presented in support of the hypothesis that chemical stimuli control the development of infection structures on the host surface by T. cucumeris. On the stem of a young radish seedling there are discrete, susceptible a·reas which become fewer and eventually disappear as the seedling ages. Rubbing the stems of radish seedlings with or without an organic solvent increases the number of infection cushions formed by a crucifor-attacking isolate, and returns an older resistant seedling to the susceptible condition. No infection cushions form on strips of cuticle and epidermis removed from the host.The susceptibility of several hosts to a number of isolates is closely correlated with the stimulation of these isolates by seedling roots enclosed in "Cellophane".In vitro investigations on "Cellophane" membranes show that root exudates from different hosts stimulate the growth of specialized and non-specialized isolates, and that under these conditions there is no correlation between specificity and stimulation.Crucifer-attacking isolates form infection cushions on artificial membranes covering intact radish seedlings, stem, or cotyledon pieces. Using a bioassay technique with collodion membranes mounted on van Tieghem rings, it is shown that exudates from radish stems and cotyledons stimulate infection cushion formation. This is the first direct evidence that the stimulant is a natural constituent of the host plant and is not produced by an interaction between host and pathogen.

No abstract