Leaf abscission and stem lesions (intumescences) on poplar clones after SO2 and O3 fumigation: a link with ethylene release?

Differences in premature leaf abscission and in visible stem injury in genetic lines of poplar followed continuous fumigations with air pollutant levels of SO2 (90-100 nl l-1) and O3 (70-80 nl l-1) either separately or together. The clones used were: Populus deltoides var. missiouriensis Marsh., P. nigra cv. ìtalica' L., and the hybrids P. nigra cv. italica' X P. deltoides (He-X/3) and P. nigra cv. ìtalica' X P. nigra cv. S̀erres' (He-K/7). While most leaf abscission occurred within 20 d from the start of fumigation, stem lesions (intumescences), appeared only after 72 d. Their anatomical characteristics include the formation of lysigenous aerenchyma in the lower parts of the intumescence, the sloughing of superficial cells from the injured area, and the development of crystalline formations on the surface of the lesions. P. deltoides exhibited the least morphological response to the gases. Ethylene released from fumigated leaves was determined at the same gas concentration of SO2 (100 nl l-1), O3 (75 nl l-1) and their mixture. Leaves of P. deltoides consistently showed the lowest ethylene production after the gas treatments. P. ìtalica' production was higher but was little altered by the treatments. The two hybrids He-X/3 and He-K/7 showed the greatest increases in ethylene evolution with time. With He-K/7 exposed to the gas mixture the production of ethylene decreased after the initial sharp rise during days 1-2, and reflected the considerable leaf damage observed after day 3. The results suggest that sensitivity to air pollution, (as shown by leaf abscission and the formation of stem intumescences) can be correlated with the level of pollutant-induced ethylene evolution from leaves. Initially high levels could induce abscission, whilst prolonged production could be responsible for intumescence initiation. The discussion proposes a series of events from SO2 and/or O3 entry into the leaf and the physiological reasons for the clonal differences.