TRANSCRIPTIONAL ACTIVATION OF PLANT DEFENSE GENES BY SHORT-TERM AIR POLLUTANT STRESS

The expression of defence genes was monitored by RNA blot analyses in tobacco plants (Nicotiana tabacum cv. SR-1) treated with various ail pollutants at realistic concentrations that prevail in urban areas. Six-week-old plants responded with an increase in the steady-state mRNA levels of phenylalanine ammonia-lyase (PAL), chalcone synthase (CHS), chitinase and beta-1,3-glucanase, when exposed to defined and subnecrotic concentrations of automobile exhaust and/or ozone over a period of 48 h. An enhanced expression of genes encoding mitochondrial and cytosolic superoxide dismutases suggested that aii pollutants induced consider able oxidative stress. Moreover, wounding or elicitor treatment of plants already exposed to automobile exhaust and/or ozone additionally increased the expression of the above defence genes, but not so in NO2. Since the main difference between NO2 and exhaust gas is the absence of the hydrocarbon compounds in the former, we regard hydrocarbons as favourite candidates for the toxic effect of exhaust gas, and they possibly act by generating an enhanced oxidative stress.