4.2.7S
HOST-PATHOGEN SYSTEMS IN A CHANGING ATMOSPHERE: CASE STUDIES WITH FUNGAL PATHOGENS ON WHEAT

AV TIEDEMANN1 and KH FIRSCHING2

1Department of Phytomedicine, Faculty of Agriculture, University of Rostock, Germany; 2GSF Research Center for Environment and Health, Munich-Neuherberg, Germany

Background and objectives
Among the best-studied factors of 'global change' are the atmospheric trace gases ozone and CO2. Both components significantly affect the physiology of plants in the range of current ambient concentrations. These physiological alterations also change the response of plants to pathogens. This paper presents data from model experiments on quantitative effects of increased ozone and CO2 concentrations on the susceptibility of wheat plants to several important leaf pathogens. The main emphasis is placed on the relevance of such experimental data with regard to the field situation, and in particular on the effects of interfering factors such as nitrogen fertilization, plant age and combination effects of elevated concentrations of both gases.

Materials and methods
Experiments were carried out in fumigation chambers under fully controlled climate conditions in plant-growth chambers. In the ozone episode studies, plants were exposed to concentrations varied between 120 and 400 mg/m3 ozone for a short period (5-7 days, 7 h per day) prior to inoculation with a leaf pathogenic fungus. Inoculated plants were generally incubated in filtered-air atmospheres to exclude direct gas effects on the pathogen. Epidemic simulation experiments with heat leaf rust (Puccinia recondita) were conducted under simulated ambient ozone profiles over a whole growth period, from seedling emergence until ripeness (122 days). Ozone levels and climate conditions followed the real outdoor situation between April 1 and July 31 of three averaged years in central Germany. The epidemic was started by an initial inoculation at growth stage 21-25 (booting). Uredospores formed in each chamber were periodically redistributed on the same plants to simulate an epidemic disease cycle. Carbon dioxide was applied at constant background concentrations of 400 or 650 ml/I.

Results and conclusions
Ozone effects on the susceptibility of wheat to three leaf mycoses were strongly affected by plant age and the status of nitrogen supply. Plants at young or mature growth stages were significantly more sensitive to ozone than plants during stem elongation. Susceptibility to leaf blotch (Septoria nodorum) was enhanced only at ozone-sensitive growth stages [1], while powdery mildew (Erysiphe graminis) was generally reduced on exposed plants. High levels of nitrogen fertilization strongly enhanced ozone effects on susceptibility of wheat to leaf blotch, while the mildew-reducing effects of ozone were partly offset. Nitrogen supply had little effect on the response of leaf rust to ozone. Thus, coincidence of high nitrogen supply and elevated ozone concentrations may particularly predispose wheat plants for fungal diseases [2].

Harmful effects of ozone on photosynthesis and yield parameters were completely compensated by elevated background CO2 levels. Leaf rust epidemic was only slightly enhanced by increased CO2, while it was strongly inhibited by elevated ozone. The reduced leaf rust infection on ozone-treated plants was due to strongly increased hypersensitive host cell responses. At the elevated level of CO2, the ozone-induced increase in plant hypersensitivity was largely lost and partly compensated the inhibiting effects of ozone on the disease. It is concluded that ozone effects on plant disease susceptibility may be strongly altered by interfering factors such as plant developmental stage, nutrient supply and other atmospheric trace gases. Alterations of ozone effects due to these interfering factors may be gradual or strong. This significantly complicates any modelling or prediction of potential atmospheric impacts on the predisposition for diseases of a particular crop plant.

References
1. Tiedemann AV, Pfahler B, 1994. Physiological and Molecular Plant Pathology 45, 153-167.
2. Tiedemann AV, 1996. Journal of Plant Diseases and Protection 103, 409-419.