Overproduction of ascorbate peroxidase in the tobacco chloroplast does not provide protection against ozone

被引:68
作者
Torsethaugen, G
Pitcher, LH
Zilinskas, BA
Pell, EJ
机构
[1] UNIV OSLO,DEPT BIOL,N-0316 OSLO,NORWAY
[2] RUTGERS STATE UNIV,COOK COLL,DEPT PLANT SCI,NEW BRUNSWICK,NJ 08903
[3] PENN STATE UNIV,DEPT PLANT PATHOL,UNIVERSITY PK,PA 16802
[4] PENN STATE UNIV,ENVIRONM RESOURCES RES INST,UNIVERSITY PK,PA 16802
关键词
D O I
10.1104/pp.114.2.529
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Transgenic tobacco (Nicotiana tabacum cv Bel W3) plants were used to test the hypothesis that protection from O-3 injury could be conferred by overproduction of ascorbate peroxidase (APX) in the chloroplast. The 10-fold increase in soluble APX activity in the chloroplast was expected to alleviate an implied increase in oxidative potential and prevent damage caused by O-3. Three different O-3 exposure experiments (one acute and two chronic) with two replicates each were conducted. APX activity in nontransgenic plants increased in response to chronic O-3 exposure. However, most responses to O-3 were similar between transgenic and nontransgenic plants. These included reductions in net photosynthesis and stomatal conductance, increases in ethylene emission and visible injury, and a decline in the level of the small subunit of ribulose-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/oxygenase quantity was observed in the chronic experiments. O-3 did not induce acceleration of senescence, as expected from studies with most other species; rather, the tobacco plants rapidly developed necrotic lesions. Thus, overproduction of APX in the chloroplast did not protect this cultivar of tobacco from O-3.
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页码:529 / 537
页数:9
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