Increased Anion Channel Activity Is an Unavoidable Event in Ozone-Induced Programmed Cell Death

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.

Ozone-induced caspase-like activities are dependent on early ion channel regulations and ROS generation inArabidopsis thalianacells

“…Our data suggest that in addition to the delayed outward rectifying K + channel activation, 2 the activation of anion channel 1 and in a minor way the Ca 2+ influx, 1 as a production of singlet oxygen possibly linked to mitochondrial dysfunction could also participate to the activation of caspase-like activities. Further studies are thus needed to understand the nature, role and regulation of the caspase-like proteins in O 3 -induced cell death.…”

“…The caspase-like activity was observed mostly in the nucleus and just feebly in the cytoplasm (Fig. 1M) 14 Since in our model DABCO, a scavenger of singlet oxygen, was also found to drastically reduce the O 3 -induced cell death and mitochondrial depolarization, 1 a classic hallmark of cell undergoing PCD and a prerequisite to release of caspase from mitochondria in animal, 15 we further test its impact on caspase-like activities. As observed for ion channel blockers, DABCO drastically reduced the caspase-like activities since no green fluorescent patches could be detected in O 3 -treated cells after DABCO pre-treatment (Fig.…”

“…[1][2][3] This consist in an oxidative dependent controlled cell death process involving cell shrinkage due to an early activation of anion channel 1 and a delayed activation of K + outward currents, 2 but also to early events like Ca 2+ influx or singlet oxygen production possibly linked to mitochondrial dysfunction. 1 Here we provide evidence that most of these early events act downstream of caspase-like activities as recently demonstrated for K + channel activation. …”

Peroxyacetyl nitrate-induced oxidative and calcium signaling events leading to cell death in ozone-sensitive tobacco cell-line

“…6 Our group has also participated to the study on the behavior of plant cells (leading to cell death) in responses to O 3 using cell suspension cultures of Arabidopsis thaliana, 7 and O 3 -sensitive and O 3 -tolerant tobacco (Nicotiana tabacum L.), 8 revealing that secondarily produced reactive oxygen species (ROS), calcium signaling events, and anion channel regulations are all involved in the O 3 -stimulated signaling leading to programmed cell death. One of key finding is that salicylic acid (SA) is involved in cell death development through regulation of signaling cascade including oxidative signaling and calcium signaling mechanisms.…”

Mitigation of copper toxicity by DNA oligomers in green paramecia

“…[1][2][3] One of key signaling events contributing to crosstalk in plant responses to abiotic stress would be transient increase in cytosolic free calcium ion concentration stimulated by generation of ROS through ROS-dependent activation of calcium channels on the vacuolar and/or plasma membranes. 1,4 Impact of various ions of transition metals, chiefly of copper, on oxidative and calcium signal transductions leading to cell death in plant cells have been documented to date. Among such metals, copper is known to be a phytotoxic metal which reportedly induces a series of biological and chemical reactions in plant cells including the burst of reactive oxygen species production and stimulation of calcium channel opening allowing a transient increase in cytosolic calcium concentrations.…”