Abstract
ABSTRACT Experiments with Arabidopsis mutants and sensitive and tolerant pairs in several other species have elucidated the molecular basis of plant ozone sensitivity and ozone lesion development. They have indicated an important role for hormonal signalling in determining the outcome of ozone challenge at the cellular level. The reactive oxygen species (ROS) from ozone degradation can cause either direct necrotic damage or induce the process of programmed cell death. Perception of ozone or ROS from its degradation in the apoplast activates several signal transduction pathways that regulate the responses of the cells to the increased oxidative load. Plant hormones salicylic acid, jasmonic acid, ethylene and abscisic acid are involved in determining the duration and extent of ozone‐induced cell death and its propagation. Salicylic acid is required for the programmed cell death, ethylene promotes endogenous ROS formation and lesion propagation, and jasmonic acid is involved in limiting the lesion spreading. Abscisic acid is most likely involved through the regulation of stomata and thus is expected to affect lesion initiation. The roles and interactions of perception of ozone, the immediate downstream responses, hormone biosynthesis and signalling during ozone lesion initiation and formation are reviewed.
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Claims 9
Claim · model-written summary
Hormonal signalling helps determine cellular ozone outcomes.
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e0“an important role for hormonal signalling in determining the outcome of ozone challenge at the cellular level”
Claim · model-written summary
Ozone derived ROS can cause necrotic damage.
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e0“The reactive oxygen species (ROS) from ozone degradation can cause either direct necrotic damage or induce the process of programmed cell death”
Claim · model-written summary
Ozone derived ROS can induce programmed cell death.
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e0“The reactive oxygen species (ROS) from ozone degradation can cause either direct necrotic damage or induce the process of programmed cell death”
Claim · model-written summary
Ozone or ROS perception activates signalling pathways regulating oxidative load response.
- Outcome
- responses of the cells to the increased oxidative loade0
- Qualifier
- signal transduction pathwayse0
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e0“Perception of ozone or ROS from its degradation in the apoplast activates several signal transduction pathways that regulate the responses of the cells to the increased oxidative load”
Claim · model-written summary
Salicylic acid is required for programmed cell death.
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Verbatim
e0“Salicylic acid is required for the programmed cell death”
Claim · model-written summary
Ethylene promotes endogenous ROS formation.
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e0“ethylene promotes endogenous ROS formation and lesion propagation”
Claim · model-written summary
Ethylene promotes lesion propagation.
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e0“ethylene promotes endogenous ROS formation and lesion propagation”
Claim · model-written summary
Jasmonic acid limits lesion spread.
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e0“jasmonic acid is involved in limiting the lesion spreading”
Claim · model-written summary
Abscisic acid likely affects lesion initiation through stomata.
Not reportedTaxon
Verbatim
e0“Abscisic acid is most likely involved through the regulation of stomata and thus is expected to affect lesion initiation”