4.2.3
THE SUSCEPTIBILITY OF POPULUS TRICHOCARPA x BALSAMIFERA TO MARSSONINA LEAF SPOT UNDER ELEVATED OZONE

JA BEARE1, SA ARCHER1 and JNB BELL1

1Imperial College at Silwood Park, Ascot, Berkshire SL5 7PY, UK

Background and objectives
Trophospheric ozone levels have been augmented by 100-200% in the northern hemisphere over the last 100 years [1]. More recently, it has been implicated as one of the most important pollutants affecting vegetation. Poplars are particularly sensitive to its effects, which include alterations in photosynthesis, cell membrane degradation and a general disruption of cell metabolism. Ultimately, these physiological disturbances result in extensive tissue damage leading to premature senescence and leaf abscission. Facultative, necrotrophic, fungal pathogens such as Marssonina, which causes leaf spot disease of poplar, thrive on senescent plant material. This has led to the suggestion that diseases caused by these pathogens are likely to be increased under elevated ozone [2]. It is also widely known that abiotic stresses such as ozone increase the production of resistance factors inhibitory to plant pathogens, particularly in young poplar leaves.

This study aims to show that the severity of blackspot disease of poplar is altered by exposure of its host to chronic levels of ozone. It is proposed that increased disease is more likely on older leaves, whilst decreases may occur on younger leaves.

Materials and methods
Rooted cuttings of Populus trichocarpa x balsamifera were fumigated with 100 p.p.b. ozone over 6 weeks. One young, upper leaf and one older, lower leaf were taken from each plant at regular intervals throughout the exposure period, and inoculated on the adaxial surface with a Marssonina tremulae spore suspension. Following incubation at ambient temperature, the diameter of the largest lesion on the leaf surface was measured across its widest point 8, 12 and 16 days after inoculation.

Results and conclusions
Daily growth increment of Marssonina lesions was significantly increased on older ozone-treated leaves, resulting in a significantly increased lesion size. Moreover, the strength of this effect increased with increased length of exposure to the pollutant. Conversely, pre-treatment of younger leaves with ozone caused a substantial increase in lesion size on leaves exposed to the pollutant for 2 weeks, but a significant decrease in lesion size on leaves exposed for 6 weeks.

It is proposed that ozone-induced tissue injury causes an increase in the severity of the disease both on older leaves and initially on younger leaves. Later reductions in the disease on newly emerged upper leaves may be attributed to an increase in the production of resistance factors, possibly as a result of systemic effects from the lower part of the plant. In an elevated ozone environment, the decreased resistance of older leaves to the disease is likely to be negated by the simultaneous increased resistance of young leaves under these conditions.

References
1. United Kingdom Photochemical Oxidants Review Group, 1987. Department of the Environment and Department of Transport. 2. Manning WJ, Tiedemann A, 1995. Environmental Pollution 88, 219-245.