OVERPRODUCTION OF ASCORBATE PEROXIDASE IN THE TOBACCO CHLOROPLAST DOES NOT PROVIDE PROTECTION AGAINST OZONE

Transgenic tobacco (Nicotiana tabacum cv Bel W3) plants were used to t est the hypothesis that protection from O-3 injury could be conferred by overproduction of ascorbate peroxidase (APX) in the chloroplast. Th e 10-fold increase in soluble APX activity in the chloroplast was expe cted to alleviate an implied increase in oxidative potential and preve nt damage caused by O-3. Three different O-3 exposure experiments (one acute and two chronic) with two replicates each were conducted. APX a ctivity in nontransgenic plants increased in response to chronic O-3 e xposure. However, most responses to O-3 were similar between transgeni c and nontransgenic plants. These included reductions in net photosynt hesis and stomatal conductance, increases in ethylene emission and vis ible injury, and a decline in the level of the small subunit of ribulo se-1,5-biphosphate carboxylase/oxygenase mRNA transcripts observed in response to the air pollutant in the acute and/or chronic experiments. No O-3-induced effect on ribulose-l,5-biphosphate carboxylase/oxygena se quantity was observed in the chronic experiments. O-3 did not induc e acceleration of senescence, as expected from studies with most other species; rather, the tobacco plants rapidly developed necrotic lesion s. Thus, overproduction of APX in the chloroplast did not protect this cultivar of tobacco from O-3.