Ozone damage and tolerance in leaves of two poplar genotypes

被引:24
|
作者
Giacomo, Bartoli [1 ,2 ]
Forino, Laura Maria Costantina [2 ]
Tagliasacchi, Anna Maria [2 ]
Bernardi, Rodolfo [1 ]
Durante, Mauro [1 ]
机构
[1] Univ Pisa, Genet Sect, Dept Agr Plant Biol, I-56124 Pisa, Italy
[2] Univ Pisa, Dept Biol, I-56126 Pisa, Italy
关键词
Leaf injury; ozone stress; Populus deltoides x maximowiczii; Eridano clone; Populus x euramericana; I-214; clone; programmed cell death (PCD); reactive oxygen species (ROS); PROGRAMMED CELL-DEATH; OXIDATIVE BURST; PLANT; SENSITIVITY; CLONES; STRESS; EXPOSURE; PHOTOSYNTHESIS; ARABIDOPSIS; RESISTANCE;
D O I
10.1080/00087114.2010.10589755
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
The effects induced by an acute ozone exposure were investigated in two poplar hybrids differentially O-3 susceptible in terms of leaf injuries: Populus deltoides x maximowiczii, Eridano clone and Populus x euramericana, I-214 clone, the sensitive and the tolerant respectively. Both the leaf anatomy and the responses induced by ozone in the leaves were analysed, using a cyto-histochemical approach. Morphoanatomical characters, such as amphistomatous lamina, higher stomatal density and relaxed mesophyll cell packing (evaluated by the palisadeness coefficient), observed in the sensitive clone leaves, may favour a greater O-3 uptake in the apoplast and increase the cumulative dose of pollutant per mesophyll cell, with respect to tolerant clone leaves. Mesophyll cells of sensitive plants were the main targets for O-3. After an acute ozone treatment, the palisade parenchyma cells showed a decrease in chloroplast number and size, resulting best suited both to perceive the stress by O-3 or reactive oxygen species and to activate several signal transduction pathways, in relation to their morphological, physiological and functional properties predisposing an efficient cell communication, signalling and stimuli sensing. The quick and well localized pattern of cell death induced by O-3 in sensitive poplar leaves was accompanied by some hallmarks of programmed cell death: nuclear shrinkage, chromatin condensation and cell wall collapse.
引用
收藏
页码:422 / 434
页数:13
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