Abstract
BackgroundOzone is a major secondary air pollutant often reaching high concentrations in urban areas under strong daylight, high temperature and stagnant high-pressure systems. Ozone in the troposphere is a pollutant that is harmful to the plant.Principal FindingsBy exposing cells to a strong pulse of ozonized air, an acute cell death was observed in suspension cells of Arabidopsis thaliana used as a model. We demonstrated that O3 treatment induced the activation of a plasma membrane anion channel that is an early prerequisite of O3-induced cell death in A. thaliana. Our data further suggest interplay of anion channel activation with well known plant responses to O3, Ca2+ influx and NADPH-oxidase generated reactive oxygen species (ROS) in mediating the oxidative cell death. This interplay might be fuelled by several mechanisms in addition to the direct ROS generation by O3; namely, H2O2 generation by salicylic and abscisic acids. Anion channel activation was also shown to promote the accumulation of transcripts encoding vacuolar processing enzymes, a family of proteases previously reported to contribute to the disruption of vacuole integrity observed during programmed cell death.SignificanceCollectively, our data indicate that anion efflux is an early key component of morphological and biochemical events leading to O3-induced programmed cell death. Because ion channels and more specifically anion channels assume a crucial position in cells, an understanding about the underlying role(s) for ion channels in the signalling pathway leading to programmed cell death is a subject that warrants future investigation.
Highlights
Ozone produced by a complex series of photochemical reactions from primary precursor emissions of nitrogen oxide and volatile organic compounds, is a major secondary air pollutant
In order to check whether this O3-induced cell death was due to an active mechanism requiring active gene expression and cellular metabolism, A. thaliana cell suspensions were treated with actinomycin D (AD), an inhibitor of RNA synthesis, or with cycloheximide (Chx), an inhibitor of protein synthesis, at 20 mg.mL21 each, 15 min prior to O3 exposure
Actinomycin D and Chx significantly reduced the O3-induced cell death (Figure 1D). These results indicated that this cell death required active cell metabolism, namely gene transcription and de novo protein synthesis
Summary
Ozone produced by a complex series of photochemical reactions from primary precursor emissions of nitrogen oxide and volatile organic compounds, is a major secondary air pollutant. A quick burst of ROS produced by plant cells is induced by high concentrations of O3 [3] and it resembles the oxidative burst of the HR in incompatible plant–pathogen interactions [7]. An exposure to O3, leads to a rapid increase in cytosolic free calcium ([Ca2+]cyt) [8,9,10] This increase in cytosolic Ca2+ concentration is sensitive to Ca2+ chelators, ion channel blockers, and ROS scavengers suggesting that calcium influx from the apoplast acts as a secondary messenger initiating oxidative cell death [4,10] in addition to rapid changes in the protein phosphorylation pattern [11]. Ozone in the troposphere is a pollutant that is harmful to the plant
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