Electrochemical Gradient Research Articles

The role of ion homeostasis in adaptation and tolerance to acetic acid stress in yeasts.

Maintenance of asymmetric ion concentrations across cellular membranes is crucial for proper yeast cellular function. Disruptions of these ionic gradients can significantly impact membrane electrochemical potential and the balance of other ions, particularly under stressful conditions such as exposure to acetic acid. This weak acid, ubiquitous to both yeast metabolism and industrial processes, is a major inhibitor of yeast cell growth in industrial settings and a key determinant of host colonization by pathogenic yeast. Acetic acid toxicity depends on medium composition, especially on the pH (H+ concentration), but also on other ions' concentrations. Regulation of ion fluxes is essential for effective yeast response and adaptation to acetic acid stress. However, the intricate interplay among ion balancing systems and stress response mechanisms still presents significant knowledge gaps. This review offers a comprehensive overview of the mechanisms governing ion homeostasis, including H+, K+, Zn2+, Fe2+/3+, and acetate, in the context of acetic acid toxicity, adaptation, and tolerance. While focus is given on Saccharomyces cerevisiae due to its extensive physiological characterization, insights are also provided for biotechnologically and clinically relevant yeast species whenever available.

Nickel nitride-mediated nitric oxide generation for combating implant-associated infections

NiTi alloys are widely used in the fabrication of biomedical implants, and it is essential to endow them with selective antibacterial properties to avoid implant-associated infection. In this study, nickel nitride (Ni3N), as a promising new inorganic nitric oxide (NO) donor, was in situ constructed on the surface of NiTi alloys through a straightforward two-step plasma immersion ion implantation (PIII) strategy. Nickel sites were first exposed by physical bombardment with argon or metal plasma, followed by reaction with nitrogen plasma to form Ni3N. Ni3N can disrupt the transmembrane proton electrochemical gradient by capturing protons to produce ammonia species (NHx), resulting in the accumulation of reactive oxygen species (ROS) as a result of bacterial metabolic disruption. On the other hand, the generated NHx can further react with ROS to produce NO and reactive nitrogen species (RNS). As a result, the Ni3N films exhibited more than 99 % antibacterial efficiency against both gram-negative and gram-positive bacteria. They also demonstrated effective antibacterial properties in a rat subcutaneous implant model. In addition, the modified NiTi alloys exhibit good corrosion resistance and cytocompatibility. This study provides a green, safe, and inexpensive method for constructing metal nitride films on implant surfaces and offers new ideas for the clinical design and fabrication of novel antibacterial implants.

Mitochondrial energy state controls AMPK-mediated foraging behavior in C. elegans.

Organisms surveil and respond to their environment using behaviors entrained by metabolic cues that reflect food availability. Mitochondria act as metabolic hubs and at the center of mitochondrial energy production is the protonmotive force (PMF), an electrochemical gradient generated by metabolite consumption. The PMF serves as a central integrator of mitochondrial status, but its role in governing metabolic signaling is poorly understood. We used optogenetics to dissipate the PMF in Caenorhabditis elegans tissues to test its role in food-related behaviors. Our data demonstrate that PMF reduction in the intestine is sufficient to initiate locomotor responses to acute food deprivation. This behavioral adaptation requires the cellular energy regulator AMP-activated protein kinase (AMPK) in neurons, not in the intestine, and relies on mitochondrial dynamics and axonal trafficking. Our results highlight a role for intestinal PMF as an internal metabolic cue, and we identify a bottom-up signaling axis through which changes in the PMF trigger AMPK activity in neurons to promote foraging behavior.

Statin-mediated reduction in mitochondrial cholesterol primes an anti-inflammatory response in macrophages by upregulating Jmjd3.

Statins are known to be anti-inflammatory, but the mechanism remains poorly understood. Here, we show that macrophages, either treated with statin in vitro or from statin-treated mice, have reduced cholesterol levels and higher expression of Jmjd3, a H3K27me3 demethylase. We provide evidence that lowering cholesterol levels in macrophages suppresses the adenosine triphosphate (ATP) synthase in the inner mitochondrial membrane and changes the proton gradient in the mitochondria. This activates nuclear factor kappa-B (NF-κB) and Jmjd3 expression, which removes the repressive marker H3K27me3. Accordingly, the epigenome is altered by the cholesterol reduction. When subsequently challenged by the inflammatory stimulus lipopolysaccharide (M1), macrophages, either treated with statins in vitro or isolated from statin-fed mice, express lower levels proinflammatory cytokines than controls, while augmenting anti-inflammatory Il10 expression. On the other hand, when macrophages are alternatively activated by IL-4 (M2), statins promote the expression of Arg1, Ym1, and Mrc1. The enhanced expression is correlated with the statin-induced removal of H3K27me3 from these genes prior to activation. In addition, Jmjd3 and its demethylase activity are necessary for cholesterol to modulate both M1 and M2 activation. We conclude that upregulation of Jmjd3 is a key event for the anti-inflammatory function of statins on macrophages.

Assessing the accuracy of TD-DFT excited-state geometries through optimal tuning with GW energy levels.

We study the accuracy of excited state (ES) geometries using optimally tuned LC-PBE functionals with tuning based on GW quasiparticle energies. We compare the results obtained with the PBE, PBE0, non-tuned, and tuned LC-PBE functionals with available high-level CC reference values as well as experimental data. First, we compare ES geometrical parameters obtained for three different types of systems: molecules composed of a few atoms, 4-(dimethylamino)benzonitrile (DMABN), and conjugated dyes. To this end, we used wave-function results as benchmarks. Next, we evaluate the accuracy of the theoretically simulated spectra as compared to the experimental ones for five large dyes. Our results show that, besides small compact molecules for which tuning LC-PBE does not allow obtaining geometries more accurate than those computed with standard functionals, tuned range-separated functionals are clearly to be favored, not only for ES geometries but also for 0-0 energies, band shapes, and intensities for absorption and emission spectra. In particular, the results indicate that GW-tuned LC-PBE functionals provide improved matching with experimental spectra as compared to conventionally tuned functionals. It is an open question whether TD-DFT with GW-tuned functionals can qualitatively mimic the actual many-body Bethe-Salpeter (BSE/GW) formalism for which analytic ionic gradients remain to be developed.

Optogenetic Determination of Dynamic and Cell-Type-Specific Inhibitory Reversal Potentials.

The reversal potential refers to the membrane potential at which the net current flow through a channel reverses direction. The reversal potential is determined by transmembrane ion gradients and, in turn, determines how the channel's activity will affect the membrane potential. Traditional investigation into the reversal potential of inhibitory ligand-gated ion channels (EInh) has relied upon the activation of endogenous receptors, such as the GABA-A receptor (GABAAR). There are, however, challenges associated with activating endogenous receptors, including agonist delivery, isolating channel responses, and the effects of receptor saturation and desensitization. Here, we demonstrate the utility of using a light-gated anion channel, stGtACR2, to probe EInh in the rodent brain. Using mice of both sexes, we demonstrate that the properties of this optically activated channel make it a suitable proxy for studying GABAAR receptor-mediated inhibition. We validate this agonist-independent optogenetic strategy in vitro and in vivo and further show how it can accurately capture differences in EInh dynamics following manipulations of endogenous ion fluxes. This allows us to explore distinct resting EInh differences across genetically defined neuronal subpopulations. Using this approach to challenge ion homeostasis mechanisms in neurons, we uncover cell-specific EInh dynamics that are supported by the differential expression of endogenous ion handling mechanisms. Our findings therefore establish an effective optical strategy for revealing novel aspects of inhibitory reversal potentials and thereby expand the repertoire of optogenetics.

Rotary FoF1-ATP Synthase-Driven Flasklike Pentosan Colloidal Motors with ATP Synthesis and Storage.

We report the hierarchical assembly of a chloroplast-derived rotary FoF1-ATPase motor-propelled flasklike pentosan colloidal motor (FPCM) with the ability of the synthesis, storage, and triggered release of biological energy currency ATP. These streamlined and submicrometer-sized hollow flasklike pentosan colloidal motors are prepared by combining a soft-template-based hydrothermal polymerization with a vacuum infusion of chloroplast-derived proteoliposomes containing rotary FoF1-ATPase motors. The generation of proton motive force across the proteoliposomes by injecting an acidic buffer solution promotes the rotation of FoF1-ATPase motors to drive the self-propelled motion of FPCMs, accompanying the inner ATP synthesis and storage. These rotary FoF1-ATPase motor-powered FPCMs exhibit a chemotactic behavior by migrating from their neck opening to their round bottom along a proton gradient of the external environment (negative chemotaxis). Such rotary biomolecular motor-driven flasklike pentosan colloidal motors with ATP synthesis and on-demand release make them promising candidates for engineering novel intelligent nanocarriers to actively regulate cellular metabolism.

Ion transport in muscle acetylcholine receptor maintained by conserved salt bridges between the pore and lipid membrane

Pores through ion channels rapidly transport small inorganic ions along their electrochemical gradients. Here, applying single-channel electrophysiology and mutagenesis to the archetypal muscle nicotinic acetylcholine receptor (AChR) channel, we show that a conserved pore-peripheral salt bridge partners with those in the other subunits to regulate ion transport. Disrupting the salt bridges in all five receptor subunits greatly decreases the amplitude of the unitary current and increases its fluctuations. However, disrupting individual salt bridges has unequal effects that depend on the structural status of the other salt bridges. The AChR ε- and δ-subunits are structurally unique in harboring a putative palmitoylation site near each salt bridge and bordering the lipid membrane. The effects of disrupting the palmitoylation sites mirror those of disrupting the salt bridges, but the effect of disrupting either of these structures depends on the structural status of the other. Thus, rapid ion transport through the AChR channel is maintained by functionally interdependent salt bridges linking the pore to the lipid membrane.

Fungal Plasma Membrane H+-ATPase: Structure, Mechanism, and Drug Discovery.

The fungal plasma membrane H+-ATPase (Pma1) pumps protons out of the cell to maintain the transmembrane electrochemical gradient and membrane potential. As an essential P-type ATPase uniquely found in fungi and plants, Pma1 is an attractive antifungal drug target. Two recent Cryo-EM studies on Pma1 have revealed its hexameric architecture, autoinhibitory and activation mechanisms, and proton transport mechanism. These structures provide new perspectives for the development of antifungal drugs targeting Pma1. In this article, we review the history of Pma1 structure determination, the latest structural insights into Pma1, and drug discoveries targeting Pma1.

Abstract LB046: Treatment of EGFR-mediated tumors via lysosome activity regulation

Abstract The lysosome is a membrane-enclosed organelle that is an essential part of the cell's digestive system. This organelle contains over 60 types of hydrolases that can break down biological polymers such as proteins, carbohydrates, lipids, and nucleic acids. These enzymes require an acidic pH for optimal function, which is achieved by using ATP hydrolysis to pump protons against their electrochemical gradient into the lysosome by the vacuolar H+ ATPase (V-ATPase). The biogenesis of lysosomes is known to be controlled by the coordination of the regulatory gene network and the lysosomal expression, which is governed by the nuclear translocation of transcription factor EB (TFEB). Lysosomes are an essential component of the inner membrane system and participate in numerous cell biological processes, such as macromolecular degradation, antigen presentation, intracellular pathogen destruction, plasma membrane repair, exosome release, cell adhesion/migration, and apoptosis. The primary function of lysosomes is to digest extracellular material that has been internalized by endocytosis and intracellular components that have been sequestered by autophagy. They recycle the unwanted cellular material as energy, providing a nutrient source for maintaining cellular homeostasis. Lysosomal activity affects the tumor microenvironment, making the tumor cells use energy more efficiently, and it is known to be increased compared to neighboring normal tissues. However, recent studies have shown that increased lysosomal activity can lead to downregulating Receptor tyrosine kinase (RTK) activity in cancer cells. RTK activity frequently occurs with mutations in EGFR in various human cancers. Thus, EGFR is currently a target for several cancer therapies. Recently, studies on EGFR-mediated tumors through lysosome regulation have been continuously conducted. According to our previous study, it has been found that lysosome inactivation suppresses the degradation of RKT, such as EGFR, and increases the expression of EGFR.EGFR is expressed in various human tumors, including gliomas and carcinomas of the lung, colon, head and neck, pancreas, breast, ovary, and kidney. Mutations, gene amplification, and protein overexpression of various pathway elements contribute to carcinogenesis and impact prognosis. Alterations within the EGFR signaling cascade, such as gene mutations, gene amplification, and protein overexpression, have been shown to contribute to colorectal carcinogenesis.[4]In this study, we will down-regulate the expression of EGFR by activating the lysosome in DLD-1, a colorectal cancer cell line. Lysosome was activated by overexpression of V-ATPase using the lentiviral system. In vitro experiments confirmed that the degradation of EGFR was actively performed in the lysosome-activated experimental group. It inhibited cancer cells' proliferation, survival, and differentiation. Targeting lysosomes may be a new approach to overcoming EGFR-mediated cancers. Citation Format: Dohyang Kim, Anlin Zhu, Jaewoo Hong. Treatment of EGFR-mediated tumors via lysosome activity regulation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(7_Suppl):Abstract nr LB046.

Perspective on Integrative Simulations of Bioenergetic Domains.

Bioenergetic processes in cells, such as photosynthesis or respiration, integrate many time and length scales, which makes the simulation of energy conversion with a mere single level of theory impossible. Just like the myriad of experimental techniques required to examine each level of organization, an array of overlapping computational techniques is necessary to model energy conversion. Here, a perspective is presented on recent efforts for modeling bioenergetic phenomena with a focus on molecular dynamics simulations and its variants as a primary method. An overview of the various classical, quantum mechanical, enhanced sampling, coarse-grained, Brownian dynamics, and Monte Carlo methods is presented. Example applications discussed include multiscale simulations of membrane-wide electron transport, rate kinetics of ATP turnover from electrochemical gradients, and finally, integrative modeling of the chromatophore, a photosynthetic pseudo-organelle.

Small Molecule IITR08367 Potentiates Antibacterial Efficacy of Fosfomycin against Acinetobacter baumannii by Efflux Pump Inhibition.

Fosfomycin is a broad-spectrum single-dose therapy approved for treating lower urinary tract infections. Acinetobacter baumannii, one of the five major UTI-causing pathogens, is intrinsically resistant to fosfomycin. Reduced uptake and active efflux are major reasons for this intrinsic resistance. AbaF, a major facilitator superfamily class of transporter in A. baumannii, is responsible for fosfomycin efflux and biofilm formation. This study describes the identification and validation of a novel small-molecule efflux pump inhibitor that potentiates fosfomycin efficacy against A. baumannii. An AbaF inhibitor screening was performed against Escherichia coli KAM32/pUC18_abaF, using the noninhibitory concentration of 24 putative efflux pump inhibitors. The inhibitory activity of IITR08367 [bis(4-methylbenzyl) disufide] against fosfomycin/H+ antiport was validated using ethidium bromide efflux, quinacrine-based proton-sensitive fluorescence, and membrane depolarization assays. IITR08367 inhibits fosfomycin/H+ antiport activity by perturbing the transmembrane proton gradient. IITR08367 is a nontoxic molecule that potentiates fosfomycin activity against clinical strains of A. baumannii and prevents biofilm formation by inhibiting efflux pump (AbaF). The IITR08367-fosfomycin combination reduced bacterial burden by > 3 log10 in kidney and bladder tissue in the murine UTI model. Overall, fosfomycin, in combination with IITR08367, holds the potential to treat urinary tract infections caused by A. baumannii.

Гомеостаз концентрацій кальцію, калію, натрію сперми бугаїв і матково-вагінального слизу корів

The difference in concentration indicators (mM) of alkali metal ions (Са2+, К+, Na+) and the calculated ratio indices (RI:1) of their pairs (Nа+:Са2+, К+:Са2+, Nа+:К+) in bull semen samples and uterine-vaginal mucus (UVM) of the Ukrainian black-spotted breed cows was determined and suggests that the ability of sperm to passively and/or actively move through the channels and ducts of the genital organs can be associated with the physicochemical processes of passive diffusion and active transport of substances that occur in the "sperm – UVM " system. The power of the energy of chemical and electrochemical concentration gradients and the power of ion pumps of the osmotic pressure of inorganic and oncotic – organic substances promotes the movement of spermatozoa to the place of their contact with the egg cell. In favor of the proposed hypothesis indicate the obtained probable (Р ˂ 0.001) results of the stoichiometry parameters of the concentrations of Ca2+ (10 vs. 6) and Na+ (62 vs. 1066 mM) of sperm and UVM, respectively. The determined difference is also illustrated by the unequal indices of ion pair concentration ratios. If their value in sperm samples is directed from the pair Na+:К+ to the pair Na+:Са2+ (1.4:1 → 5:1 →6:1), then in the samples of UVM – from К+:Са2+ to Na+: Ca2+ (8:1 → 23:1 → 193:1). The difference in indices of a number of pairs (К+:Са2+ → Nа+:К+ → Nа+:Са2+) of sperm and UVM is directed from a smaller to a larger value (3:1 ˂ 22:1 ˂ 187:1). If the calculated changes are expressed as percentages, then the difference in indicators in the samples of the UVM, respectively, is 41; 94 and 97 %, which is in 2; 16 and 30 times more than sperm samples. This may mean that the determined significant difference in the physical and chemical state of organic and inorganic substances in the environment of the channels and ducts of the genital organs of cows creates conditions that contribute to the active and passive movement of sperm through the channels and ducts of their genital organs

A pgr5 suppressor screen uncovers two distinct suppression mechanisms and links cytochrome b6f complex stability to PGR5.

PROTON GRADIENT REGULATION5 (PGR5) is thought to promote cyclic electron flow, and its deficiency impairs photosynthetic control and increases photosensitivity of photosystem (PS) I, leading to seedling lethality under fluctuating light (FL). By screening for Arabidopsis (Arabidopsis thaliana) suppressor mutations that rescue the seedling lethality of pgr5 plants under FL, we identified a portfolio of mutations in 12 different genes. These mutations affect either PSII function, cytochrome b6f (cyt b6f) assembly, plastocyanin (PC) accumulation, the CHLOROPLAST FRUCTOSE-1,6-BISPHOSPHATASE1 (cFBP1), or its negative regulator ATYPICAL CYS HIS-RICH THIOREDOXIN2 (ACHT2). The characterization of the mutants indicates that the recovery of viability can in most cases be explained by the restoration of PSI donor side limitation, which is caused by reduced electron flow to PSI due to defects in PSII, cyt b6f, or PC. Inactivation of cFBP1 or its negative regulator ACHT2 results in increased levels of the NADH dehydrogenase-like complex. This increased activity may be responsible for suppressing the pgr5 phenotype under FL conditions. Plants that lack both PGR5 and DE-ETIOLATION-INDUCED PROTEIN1 (DEIP1)/NEW TINY ALBINO1 (NTA1), previously thought to be essential for cyt b6f assembly, are viable and accumulate cyt b6f. We suggest that PGR5 can have a negative effect on the cyt b6f complex and that DEIP1/NTA1 can ameliorate this negative effect.

The role of Na+-coupled bicarbonate transporters (NCBT) in health and disease.

Cellular and organism survival depends upon the regulation of pH, which is regulated by highly specialized cell membrane transporters, the solute carriers (SLC) (For a comprehensive list of the solute carrier family members, see: https://www.bioparadigms.org/slc/ ). The SLC4 family of bicarbonate (HCO3-) transporters consists of ten members, sorted by their coupling to either sodium (NBCe1, NBCe2, NBCn1, NBCn2, NDCBE), chloride (AE1, AE2, AE3), or borate (BTR1). The ionic coupling of SLC4A9 (AE4) remains controversial. These SLC4 bicarbonate transporters may be controlled by cellular ionic gradients, cellular membrane voltage, and signaling molecules to maintain critical cellular and systemic pH (acid-base) balance. There are profound consequences when blood pH deviates even a small amount outside the normal range (7.35-7.45). Chiefly, Na+-coupled bicarbonate transporters (NCBT) control intracellular pH in nearly every living cell, maintaining the biological pH required for life. Additionally, NCBTs have important roles to regulate cell volume and maintain salt balance as well as absorption and secretion of acid-base equivalents. Due to their varied tissue expression, NCBTs have roles in pathophysiology, which become apparent in physiologic responses when their expression is reduced or genetically deleted. Variations in physiological pH are seen in a wide variety of conditions, from canonically acid-base related conditions to pathologies not necessarily associated with acid-base dysfunction such as cancer, glaucoma, or various neurological diseases. The membranous location of the SLC4 transporters as well as recent advances in discovering their structural biology makes them accessible and attractive as a druggable target in a disease context. The role of sodium-coupled bicarbonate transporters in such a large array of conditions illustrates the potential of treating a wide range of disease states by modifying function of these transporters, whether that be through inhibition or enhancement.

“Transforming enemy into friend” strategy-based stimuli responsive dual-drug liposomes for synergistic chemo-photodynamic therapy

Photodynamic therapy (PDT) induces aggravation of tumor hypoxia, which leads to worsening tumor invasiveness and metastasis. Combining hypoxia-responsive prodrugs with photosensitizers could transform “enemy” (tumor hypoxia) into “friend” (positive amplifier) to facilitate efficient activation of prodrugs. However, it remains challenging to develop a highly effective co-delivery nanoplatform due to the poor compatibility between vehicles and cargoes. Herein, we selected podophyllotoxin (PPT) as a model drug to synthesize hypoxia-responsive polyphenol prodrug (PAG). By introducing a chemical modification strategy, PAG and Chlorin e6 (Ce6) could be remotely co-encapsulated into liposomes (PAG/Ce6 LPs) at a synergistic ratio utilizing metal ions gradient. In vitro experiments demonstrated that PAG/Ce6 LPs could kill tumor cells through multiple pathways; i) generating reactive oxygen species (ROS) for direct cell killing; ii) consuming intracellular glutathione (GSH) to disturb intracellular redox homeostasis to induce tumor cell apoptosis. iii) aggravating hypoxia micro-environment to promote PPT release for chemotherapy. Furthermore, the excellent stability of PAG/Ce6 LPs guaranteed extended drug blood circulation time, enhanced tumor accumulation and improved anticancer efficacy. Additionally, PAG/Ce6 LPs kept fluorescence quench in circulation and specifically recovered at the tumor site, avoiding the obstacle of phototoxicity. Such a co-delivery nanoplatform, integrating hypoxia-responsive polyphenol prodrugs and photosensitizer into one nanocarrier, provides new insight into solving the challenges of chemo-photodynamic therapy.

Modelling energy-harvesting processes in primitive cells: Proton transport across bilayers driven by the oxidation of sulfite

A frequently debated topic related to the origin of life centers around the question of how complex forms of life on today's Earth may have evolved over time from simpler predecessors. For example, the question of how proton concentration gradients across cellular membranes developed in ancestral protocells remains unanswered. This process, which is indispensable for the generation of chemical energy in modern organisms, is driven by energy derived from redox processes in the respiratory chain. Since it is highly unlikely that the complex machinery of the respiratory chain was available on early Earth, we provide an example of how proton gradients can be established in less complex systems. Utilizing liposomes as models of primitive cells, we were able to generate proton gradients of about two pH units across the liposome bilayers using redox reactions as the driving force. Electrons were transferred from sodium sulfite present on the outside of the liposomes to ferricyanide, which was trapped on the inside. A lipid-soluble phenazine derivative served as a shuttle that transferred both electrons and protons across the lipid bilayer. Because sulfite would have been an abundant reduced solute available to the earliest cells, we propose that it may have been a primary source of redox energy for primitive chemiosmotic energy transduction.

Synthesis of Raspberry-like Nanoparticles via Surface Grafting of Positively Charged Polyelectrolyte Brushes: Colloidal Stability and Surface Properties.

A method to synthesize stable, raspberry-like nanoparticles (NPs), using surface grafting of poly(glycidyl methacrylate) (PGMA) brushes on a polystyrene (PS) core with varying grafting densities, is reported. A two-step functionalization reaction of PGMA epoxide groups comprising an amination step first using ethylene diamine and then followed by a quaternization using glycidyltrimethylammonium chloride generates permanently and positively charged polyelectrolyte brushes, which result in both steric and electrostatic stabilization. The dispersion stability of the brush-bearing NPs is dramatically improved compared to that of the pristine PS core in salt solutions at ambient (25 °C) and elevated temperatures (60 °C). Additionally, the grafted polyelectrolyte chains undergo a reversible swelling in the presence of different ionic strength (IS) salts, which modulate the surface properties, including roughness, stiffness, and adhesion. An atomic force microscope under both dry and wet conditions was used to image conformational changes of the polyelectrolyte chains during the swelling and deswelling transitions as well as to probe the nanomechanical properties by analyzing the corresponding force-sample separation curves. The quaternized polyelectrolyte brushes undergo a conformational transition from a collapsed state to a swelled state in the osmotic brush (OB) regime triggered by the osmotic gradient of mobile ions to the interior of the polymer chain. At IS ∼ 1 M, the brushes contract and the globules reform (salted brush state) as evidenced by an increase in the surface roughness and a reduction in the adhesion of the brushes. Beyond IS ∼ 1 M, quartz crystal microbalance with dissipation monitoring measurements show that salt uptake continues to take place predominantly on the exterior surface of the brush since salt adsorption is not accompanied by a size increase as measured by dynamic light scattering. The study adds new insights into our understanding of the behavior of NPs bearing salt-responsive polyelectrolyte brushes with adaptive swelling thresholds that can ultimately modulate surface properties.

Spatial variability of and effect of light on the cœlenteron pH of a reef coral

Coral reefs, the largest bioconstruction on Earth, are formed by calcium carbonate skeletons of corals. Coral skeleton formation commonly referred to as calcification occurs in a specific compartment, the extracellular calcifying medium (ECM), located between the aboral ectoderm and the skeleton. Calcification models often assume a direct link between the surrounding seawater and the ECM. However, the ECM is separated from the seawater by several tissue layers and the cœlenteron, which contains the cœlenteric fluid found in both polyps and cœnosarc (tissue connecting the polyps). Symbiotic dinoflagellate-containing cells line the cœlenteron and their photosynthetic activity contributes to changes in the chemistry of the cœlenteric fluid, particularly with respect to pH. The aim of our study is to compare cœlenteron pH between the cœnosarc and polyps and to compare areas of high or low dinoflagellate density based on tissue coloration. To achieve this, we use liquid ion exchange (LIX) pH microsensors to profile pH in the cœlenteron of polyps and the cœnosarc in different regions of the coral colony in light and darkness. We interpret our results in terms of what light and dark exposure means for proton gradients between the ECM and the coelenteron, and how this could affect calcification.

Ion and lipid orchestration of secondary active transport.

Transporting small molecules across cell membranes is an essential process in cell physiology. Many structurally diverse, secondaryactive transporters harness transmembrane electrochemical gradients of ions to power the uptake or efflux of nutrients, signalling molecules, drugs and other ions across cell membranes. Transporters reside in lipid bilayers on the interface between two aqueous compartments, where they are energized and regulated by symported, antiported and allosteric ions on both sides of the membrane and the membrane bilayer itself. Here we outline the mechanisms by which transporters couple ion and solute fluxes and discuss how structural and mechanistic variations enable them to meet specific physiological needs and adapt to environmental conditions. We then consider how general bilayer properties and specific lipid binding modulate transporter activity. Together, ion gradients and lipid properties ensure the effective transport, regulation and distribution of small molecules across cell membranes.