Gating of aquaporins by heavy metals in Allium cepa L. epidermal cells

Changes in the water permeability, aquaporin (AQP) activity, of leaf cells were investigated in response to different heavy metals (Zn2+, Pb2+, Cd2+, Hg2+). The cell pressure probe experiments were performed on onion epidermal cells as a model system. Heavy metal solutions at different concentrations (0.05 μM–2 mM) were used in our experiments. We showed that the investigated metal ions can be arranged in order of decreasing toxicity (expressed as a decrease in water permeability) as follows: Hg>Cd>Pb>Zn. Our results showed that β-mercaptoethanol treatment (10 mM solution) partially reverses the effect of AQP gating. The magnitude of this reverse differed depending on the metal and its concentration. The time course studies of the process showed that the gating of AQPs occurred within the first 10 min after the application of a metal. We also showed that after 20–40 min from the onset of metal treatment, the water flow through AQPs stabilized and remained constant. We observed that irrespective of the metal applied, the effect of AQP gating can be recorded within the first 10 min after the administration of metal ions. More generally, our results indicate that the toxic effects of investigated metal ions on the cellular level may involve AQP gating

Microbial homoserine lactones (AHLs) are effectors of root morphological changes in barley.

While colonizing the rhizosphere, bacterial intra- and inter-specific communication is accomplished by N-Acyl-homoserine-lactones (AHLs) in a density-dependent manner. Moreover, plants are naturally exposed to AHLs and respond with tissue-specificity. In the present study, we investigated the influence of N-hexanoyl- (C6-HSL), N-octanoyl- (C8-HSL) and N-dodecanoyl-D/L-homoserine lactone (C12-HSL) on growth and root development in barley (Hordeum vulgare L.), and identified initial reactions in root cells after AHL exposures using physiological, staining, and electrophysiological methods. Treatment with short- and long-chain AHLs modulated plant growth and branched root architecture and induced nitric oxide (NO) accumulation in the calyptra and root elongation zone of excised roots in an AHL derivative-independent way. Additionally, C6- and C8-HSL treatments stimulated K+ uptake in root cells only at certain concentrations, whereas all tested concentrations of C12-HSL induced K+ uptake. In further experiments, C8-HSL promoted membrane hyperpolarization in epidermal root cells. Thus, we conclude AHLs promote plant growth and lateral root formation, and cause NO accumulation as an early response to AHLs. Furthermore, the AHL-mediated membrane hyperpolarization is leading to increased K+ uptake of the root tissue

Calcium- and potassium-permeable plasma membrane transporters are activated by copper in Arabidopsis root tips: linking copper transport with cytosolic hydroxyl radical production

Transition metals such as copper can interact with ascorbate or hydrogen peroxide to form highly reactive hydroxyl radicals (OH.), with numerous implications to membrane transport activity and cell metabolism. So far, such interaction was described for extracellular (apoplastic) space but not cytosol. Here, a range of advanced electrophysiological and imaging techniques were applied to Arabidopsis thaliana plants differing in their copper-transport activity: Col-0, high-affinity copper transporter COPT1-overexpressing (C1OE) seedlings, and T-DNA COPT1 insertion mutant (copt1). Low Cu concentrations (10μm) stimulated a dose-dependent Gd3+ and verapamil sensitive net Ca2+ influx in the root apex but not in mature zone. C1OE also showed a fivefold higher Cu-induced K+ efflux at the root tip level compared with Col-0, and a reduction in basal peroxide accumulation at the root tip after copper exposure. Copper caused membrane disruptions of the root apex in C1OE seedlings but not in copt1 plants; this damage was prevented by pretreatment with Gd3+. Our results suggest that copper transport into cytosol in root apex results in hydroxyl radical generation at the cytosolic side, with a consequent regulation of plasma membrane OH.-sensitive Ca2+ and K+ transport systems