Post‐transcriptional regulation of GORK channels by superoxide anion contributes to increases in outward‐rectifying K+ currents. Issue 4 (20th March 2013)

• Record Type: Journal Article
• Authors: Tran, Daniel; El‐Maarouf‐Bouteau, Hayat; Rossi, Marika; Biligui, Bernadette; Briand, Joël; Kawano, Tomonori; Mancuso, Stefano; Bouteau, François
• Is Part Of: New phytologist. Volume 198:Issue 4(2013)
• Page Start: 1039
• Page End: 1048
• Publication Date: 2013-03-20
• Subjects: Arabidopsis thaliana -- cell death -- GORK -- ozone -- reactive oxygen species (ROS); Botany -- Periodicals; 580
• DOI: 10.1111/nph.12226
• Languages: English
• ISSNs: 0028-646X

Abstract

Summary: Ion fluxes are ubiquitous processes in the plant and animal kingdoms, controlled by fine‐tuned regulations of ion channel activity. Yet the mechanism that cells employ to achieve the modification of ion homeostasis at the molecular level still remains unclear. This is especially true when it comes to the mechanisms that lead to cell death. In this study, Arabidopsis thaliana cells were exposed to ozone (O3 ). Ion flux variations were analyzed by electrophysiological measurements and their transcriptional regulation by RT‐PCR. Reactive oxygen species (ROS) generation was quantified by luminescence techniques and caspase‐like activities were investigated by laser confocal microscopy. We highlighted the delayed activation of K + outward‐rectifying currents after an O3 ‐induced oxidative stress leading to programmed cell death (PCD). Caspase‐like activities are detected under O3 exposure and could be decreased by K + channel blocker. Molecular experiments revealed that the sustained activation of K + outward current could be the result of an unexpected O 2 · − post‐transcriptional regulation of the guard cell outward‐rectifying K + (GORK) channels. This consists of a likely new mode of regulating the processing of the GORK mRNA, in a ROS‐dependent manner, to allow sustained K + effluxes during PCD. These data provide new mechanistic insights into K + channel regulation during an oxidative stress response.