membrane depolarization
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2021 ◽  
Vol 12 ◽  
Author(s):  
Richard T. Lamar ◽  
Hiarhi Monda ◽  
Rachel Sleighter

We report the results of a structure-activity relationship study that was undertaken to identify humic substance chemistries that drive the plant biostimulant response. The effects of seven extensively chemically characterized, ore-derived humic acids (HA) on corn seedling biomass and root and shoot morphological parameters were investigated. Chemometric analyses were then conducted to identify correlations between HA chemical features and plant biomass and morphological characteristics. The primary chemical driver of plant biomass and morphology was the ratio between HA electron accepting capacity (EAC) and electron donating capacity (EDC). The HA electron accepting capacity is found in quinones and semiquinone free radicals, while the HA electron donating capacity is found in polyphenolics and glycosylated polyphenolics. Based on our results, we propose a mechanism of action for ore-derived HA plant biostimulation that involves the interplay of pro-oxidants, in the form of quinones and semiquinone radicals, and antioxidants, in the form of polyphenols and possibly glycones and carbohydrates. The quinones/semiquinones initiate an oxidative stress response via the stimulation of transmembrane electron flow that results in both reactive oxygen species (ROS) production (i.e., an oxidative burst) and membrane depolarization, the latter of which allows Ca2+ flux from the apoplast into the cytoplasm. Based on the magnitude of depolarization, a specific cytoplasmic Ca2+ signature is produced. As a secondary messenger Ca2+, via binding to Ca2+− sensor proteins, transmits the signature signal, resulting in specific intracellular responses that include changes to plant morphology. The greater the EAC, the greater the ROS production and magnitude of plasma membrane depolarization and resulting stress response. The HA antioxidants are able to scavenge and quench the ROS and thus modulate the intensity and extent of the stress response to greater or lesser degrees, based on their concentrations and radical scavenging efficiencies, and thus modify the Ca2+ signature and ultimately the intracellular molecular responses.


2021 ◽  
Author(s):  
Maria A Neginskaya ◽  
Sally E Morris ◽  
Evgeny V Pavlov

Mitochondrial permeability transition is caused by the opening of the Cyclosporin A (CSA) dependent calcium-induced large pore, known as the Permeability Transition Pore (PTP). PTP activation is believed to be a central event in stress-induced cell death. However, the molecular details of PTP opening remain incompletely understood. PTP opening makes mitochondrial inner membrane permeable to the molecules up to 1.5 kDa in size. Solute equilibration with the media in combination with swelling due to the PTP opening make mitochondria optically transparent, a phenomenon that has been widely used as a bona fide "light-scattering" PTP detection method in isolated mitochondria. Here, we utilized holographic microscopy imaging to monitor mitochondrial optical density changes that occur during solute equilibration between matrix and cytoplasm and thus enabled us to assess PTP induction in living cells. This approach relies on label-free, real-time mitochondrial visualization due to refractive index (RI) differences between the mitochondrial matrix and cytoplasm in the intact cells. PTP activation was detected as the decrease in mitochondrial RI. These measurements were done in parallel with measurements of the mitochondrial membrane potential, using the fluorescent probe TMRM. In intact HAP 1 cells, we found that calcium stress caused CSA-sensitive depolarization of the mitochondrial inner membrane. Unexpectedly, high-conductance PTP did not occur until after nearly complete mitochondrial membrane depolarization. In cells lacking c and δ subunits of the ATP synthase, we observed calcium-induced and CSA-sensitive depolarization but not high-conductance PTP. We demonstrate that holographic imaging is a powerful novel tool with unique capabilities that allow measurement of PTP in living cells with high temporal and spatial resolution. We conclude that contrary to the widely accepted view, in living cells, high-conductance PTP is not the cause of calcium-induced membrane depolarization. Further, we provide direct evidence that ATP synthase is essential for high-conductance PTP, but not for calcium-induced CSA-sensitive membrane depolarization. We propose that PTP activation occurs as a two-phase process, where the first phase of the initial membrane depolarization is followed by the second phase of large pore opening that results in high-amplitude membrane permeabilization.


2021 ◽  
Vol 154 (1) ◽  
Author(s):  
Zhuyuan Chen ◽  
Sheng Lin ◽  
Tianze Xie ◽  
Jin-Ming Lin ◽  
Cecilia M. Canessa

Proton-gated ion channels conduct mainly Na+ to induce postsynaptic membrane depolarization. Finding the determinants of ion selectivity requires knowledge of the pore structure in the open conformation, but such information is not yet available. Here, the open conformation of the hASIC1a channel was computationally modeled, and functional effects of pore mutations were analyzed in light of the predicted structures. The open pore structure shows two constrictions of similar diameter formed by the backbone of the GAS belt and, right beneath it, by the side chains of H28 from the reentrant loop. Models of nonselective mutant channels, but not those that maintain ion selectivity, predict enlargement of the GAS belt, suggesting that this motif is quite flexible and that the loss of stabilizing interactions in the central pore leads to changes in size/shape of the belt. Our results are consistent with the “close-fit” mechanism governing selectivity of hASIC1a, wherein the backbone of the GAS substitutes at least part of the hydration shell of a permeant ion to enable crossing the pore constriction.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Junior Bernardo Molina-Hernandez ◽  
Antonio Aceto ◽  
Tonino Bucciarelli ◽  
Domenico Paludi ◽  
Luca Valbonetti ◽  
...  

AbstractThis work highlights how our silver ultra nanoclusters (ARGIRIUM-SUNc) hand-made synthesized, are very useful as a bactericide and anti-biofilm agent. The Argirium-SUNc effective antibacterial concentrations are very low (< 1 ppm) as compared to the corresponding values reported in the literature. Different bacterial defense mechanisms are observed dependent on ARGIRIUM-SUNc concentrations. Biochemical investigations (volatilome) have been performed to understand the pathways involved in cell death. By using fluorescence techniques and cell viability measurements we show, for the first time, that membrane depolarization and calcium intracellular level are both primary events in bacteria death. The ARGIRIUM-SUNc determined eradication of different biofilm at a concentration as low as 0.6 ppm. This suggests that the effect of the nanoparticles follows a common mechanism in different bacteria. It is highly probable that the chemical constitution of the crosslinks could be a key target in the disrupting mechanism of our nanoparticles. Since the biofilms and their constituents are essential for bacterial survival in contact with humans, the silver nanoparticles represent a logical target for new antibacterial treatments.


Membranes ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 851
Author(s):  
Lubna Khreesha ◽  
Abdallah Barjas Qaswal ◽  
Baheth Al Omari ◽  
Moath Ahmad Albliwi ◽  
Omar Ababneh ◽  
...  

Lithium imposes several cellular effects allegedly through multiple physiological mechanisms. Membrane depolarization is a potential unifying concept of these mechanisms. Multiple inherent imperfections of classical electrophysiology limit its ability to fully explain the depolarizing effect of lithium ions; these include incapacity to explain the high resting permeability of lithium ions, the degree of depolarization with extracellular lithium concentration, depolarization at low therapeutic concentration, or the differences between the two lithium isotopes Li-6 and Li-7 in terms of depolarization. In this study, we implemented a mathematical model that explains the quantum tunneling of lithium ions through the closed gates of voltage-gated sodium channels as a conclusive approach that decodes the depolarizing action of lithium. Additionally, we compared our model to the classical model available and reported the differences. Our results showed that lithium can achieve high quantum membrane conductance at the resting state, which leads to significant depolarization. The quantum model infers that quantum membrane conductance of lithium ions emerges from quantum tunneling of lithium through the closed gates of sodium channels. It also differentiates between the two lithium isotopes (Li-6 and Li-7) in terms of depolarization compared with the previous classical model. Moreover, our study listed many examples of the cellular effects of lithium and membrane depolarization to show similarity and consistency with model predictions. In conclusion, the study suggests that lithium mediates its multiple cellular effects through membrane depolarization, and this can be comprehensively explained by the quantum tunneling model of lithium ions.


2021 ◽  
Vol 12 ◽  
Author(s):  
Yewon Nam ◽  
Eunhye Goo ◽  
Yongsung Kang ◽  
Ingyu Hwang

The rice pathogen Burkholderia glumae uses amino acids as a principal carbon source and thus produces ammonia in amino acid-rich culture medium such as Luria–Bertani (LB) broth. To counteract ammonia-mediated environmental alkaline toxicity, the bacterium produces a public good, oxalate, in a quorum sensing (QS)-dependent manner. QS mutants of B. glumae experience alkaline toxicity and may undergo cell death at the stationary phase when grown in LB medium. Here, we show that the cell-death processes of QS mutants due to alkaline environmental conditions are similar to the apoptosis-like cell death reported in other bacteria. Staining QS mutants with bis-(1,3-dibutylbarbituric acid)-trimethine oxonol revealed membrane depolarization. CellROX™ staining showed excessive generation of reactive oxygen species (ROS) in QS mutants. The expression of genes encoding HNH endonuclease (BGLU_1G15690), oligoribonuclease (BGLU_1G09120), ribonuclease E (BGLU_1G09400), and Hu-beta (BGLU_1G13530) was significantly elevated in QS mutants compared to that in wild-type BGR1, consistent with the degradation of cellular materials as observed under transmission electron microscopy (TEM). A homeostatic neutral pH was not attainable by QS mutants grown in LB broth or by wild-type BGR1 grown in an artificially amended alkaline environment. At an artificially adjusted alkaline pH, wild-type BGR1 underwent apoptosis-like cell death similar to that observed in QS mutants. These results show that environmental alkaline stress interferes with homeostatic neutral cellular pH, induces membrane depolarization, and causes apoptosis-like cell death in B. glumae.


BIOspektrum ◽  
2021 ◽  
Vol 27 (6) ◽  
pp. 601-603
Author(s):  
Michael M. Wudick

AbstractBeing sessile, plants are exposed to adverse stresses, including wounding by insects. Albeit lacking experimental evidence, one hypothesis predicted involvement of hydro-electric signals in wound signaling. Now, we could show that the mechanosensitive anion channel MSL10 is necessary for wound-induced long-distance signaling in plants. By linking mechano-sensing, ion fluxes, membrane depolarization and electrical signal propagation, MSL10 might integrate hydraulic and electric wound signals.


Author(s):  
Juan J. Ferreira ◽  
Pascale Lybaert ◽  
Lis C. Puga-Molina ◽  
Celia M. Santi

To fertilize an egg, mammalian sperm must undergo capacitation in the female genital tract. A key contributor to capacitation is the calcium (Ca2+) channel CatSper, which is activated by membrane depolarization and intracellular alkalinization. In mouse epididymal sperm, membrane depolarization by exposure to high KCl triggers Ca2+ entry through CatSper only in alkaline conditions (pH 8.6) or after in vitro incubation with bicarbonate (HCO3–) and bovine serum albumin (capacitating conditions). However, in ejaculated human sperm, membrane depolarization triggers Ca2+ entry through CatSper in non-capacitating conditions and at lower pH (&lt; pH 7.4) than is required in mouse sperm. Here, we aimed to determine the mechanism(s) by which CatSper is activated in mouse and human sperm. We exposed ejaculated mouse and human sperm to high KCl to depolarize the membrane and found that intracellular Ca2+ concentration increased at pH 7.4 in sperm from both species. Conversely, intracellular Ca2+ concentration did not increase under these conditions in mouse epididymal or human epididymal sperm. Furthermore, pre-incubation with HCO3– triggered an intracellular Ca2+ concentration increase in response to KCl in human epididymal sperm. Treatment with protein kinase A (PKA) inhibitors during exposure to HCO3– inhibited Ca2+ concentration increases in mouse epididymal sperm and in both mouse and human ejaculated sperm. Finally, we show that soluble adenylyl cyclase and increased intracellular pH are required for the intracellular Ca2+ concentration increase in both human and mouse sperm. In summary, our results suggest that a conserved mechanism of activation of CatSper channels is present in both human and mouse sperm. In this mechanism, HCO3– in semen activates the soluble adenylyl cyclase/protein kinase A pathway, which leads to increased intracellular pH and sensitizes CatSper channels to respond to membrane depolarization to allow Ca2+ influx. This indirect mechanism of CatSper sensitization might be an early event capacitation that occurs as soon as the sperm contact the semen.


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