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.

Oxalic acid is thought to be a key factor of the early pathogenicity stage in a wide range of necrotrophic fungi. Studies were conducted to determine whether oxalate could induce programmed cell death (PCD) in Arabidopsis thaliana suspension cells and to detail the transduction of the signalling pathway induced by oxalate. Arabidopsis thaliana cells were treated with millimolar concentrations of oxalate. Cell death was quantified and ion flux variations were analysed from electrophysiological measurements. Involvement of the anion channel and ethylene in the signal transduction leading to PCD was determined by using specific inhibitors. Oxalic acid induced a PCD displaying cell shrinkage and fragmentation of DNA into internucleosomal fragments with a requirement for active gene expression and de novo protein synthesis, characteristic hallmarks of PCD. Other responses generally associated with plant cell death, such as anion effluxes leading to plasma membrane depolarization, mitochondrial depolarization, and ethylene synthesis, were also observed following addition of oxalate. The results show that oxalic acid activates an early anionic efflux which is a necessary prerequisite for the synthesis of ethylene and for the PCD in A. thaliana cells.

Summary• Fusaric acid (FA) is a toxin produced by Fusarium species. Most studies on FA have reported toxic effects (for example, alteration of cell growth, mitochondrial activity and membrane permeability) at concentrations greater than 10 − 5 M . FA participates in fungal pathogenicity by decreasing plant cell viability. However, FA is also produced by nonpathogenic Fusarii , potential biocontrol agents of vascular wilt fusaria. The aim of this study was to determine whether FA, at nontoxic concentrations, could induce plant defence responses.• Nontoxic concentrations of FA were determined from cell-growth and O 2 -uptake measurements on suspensions of Arabidopsis thaliana cells. Ion flux variations were analysed from electrophysiological and pH measurements. H 2 O 2 and cytosolic calcium were quantified by luminescence techniques.• FA at nontoxic concentrations (i.e. below 10 − 6 M ) was able to induce the synthesis of phytoalexin, a classic delayed plant response to pathogen. FA could also induce rapid responses putatively involved in signal transduction, such as the production of reactive oxygen species, and an increase in cytosolic calcium and ion channel current modulations.• FA can thus act as an elicitor at nanomolar concentrations.