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K+ is an essential cation and the most abundant in plant cells. After N, its corresponding element, K, is the nutrient required in the largest amounts by plants. Despite the numerous roles of K in crop production, improvements in the uptake and efficiency of use of K have not been major focuses in conventional or transgenic breeding studies in the past. In research on the mineral nutrition of plants in general, and K in particular, this nutrient has been shown to be essential to soil-dwelling-microorganisms (fungi, bacteria, protozoa, nematodes, etc.) that form mutualistic associations and that can influence the availability of mineral nutrients for plants. Therefore, this article aims to provide an overview of the role of soil microorganisms in supplying K+ to plants, considering both the potassium-solubilizing microorganisms and the potassium-facilitating microorganisms that are in close contact with the roots of plants. These microorganisms can influence the active transporter-mediated transfer of K+. Regarding the latter group of microorganisms, special focus is placed on the role of endophytic fungus. This review also includes a discussion on productivity through sustainable agriculture.

Long QT syndrome, short QT syndrome, Brugada syndrome and catecholaminergic polymorphic ventricular tachycardia are inherited primary electrical disorders that predispose to sudden cardiac death in the absence of structural heart disease. Also known as cardiac channelopathies, primary electrical disorders respond to mutations in genes encoding cardiac ion channels and/or their regulatory proteins, which result in modifications in the cardiac action potential or in the intracellular calcium handling that lead to electrical instability and life-threatening ventricular arrhythmias. These disorders may have low penetrance and expressivity, making clinical diagnosis often challenging. However, because sudden cardiac death might be the first presenting symptom of the disease, early diagnosis becomes essential. Genetic testing might be helpful in this regard, providing a definite diagnosis in some patients. Yet important limitations still exist, with a significant proportion of patients remaining with no causative mutation identifiable after genetic testing. This review aims to provide the latest knowledge on the genetic basis of cardiac channelopathies and discuss the role of the affected proteins in the pathophysiology of each one of these diseases.

K(+) is an essential macronutrient for plants. It is acquired by specific uptake systems located in roots. Although the concentrations of K(+) in the soil solution are widely variable, K(+) nutrition is secured by uptake systems that exhibit different affinities for K(+). Two main systems have been described for root K(+) uptake in several species: the high-affinity HAK5-like transporter and the inward-rectifier AKT1-like channel. Other unidentified systems may be also involved in root K(+) uptake, although they only seem to operate when K(+) is not limiting. The use of knock-out lines has allowed demonstrating their role in root K(+) uptake in Arabidopsis and rice. Plant adaptation to the different K(+) supplies relies on the finely tuned regulation of these systems. Low K(+)-induced transcriptional up-regulation of the genes encoding HAK5-like transporters occurs through a signal cascade that includes changes in the membrane potential of root cells and increases in ethylene and reactive oxygen species concentrations. Activation of AKT1 channels occurs through phosphorylation by the CIPK23/CBL1 complex. Recently, activation of the Arabidopsis HAK5 by the same complex has been reported, pointing to CIPK23/CBL as a central regulator of the plant's adaptation to low K(+). Na(+) is not an essential plant nutrient but it may be beneficial for some plants. At low concentrations, Na(+) improves growth, especially under K(+) deficiency. Thus, high-affinity Na(+) uptake systems have been described that belong to the HKT and HAK families of transporters. At high concentrations, typical of saline environments, Na(+) accumulates in plant tissues at high concentrations, producing alterations that include toxicity, water deficit and K(+) deficiency. Data concerning pathways for Na(+) uptake into roots under saline conditions are still scarce, although several possibilities have been proposed. The apoplast is a significant pathway for Na(+) uptake in rice grown under salinity conditions, but in other plant species different mechanisms involving non-selective cation channels or transporters are under discussion.

Williams–Beuren syndrome (WBS) is a rare genetic multisystemic disorder characterized by mild-to-moderate intellectual disability and hypersocial phenotype, while the most life-threatening features are cardiovascular abnormalities. Nowadays, there are no pharmacological treatments to directly ameliorate the main traits of WBS. The endocannabinoid system (ECS), given its relevance for both cognitive and cardiovascular function, could be a potential druggable target in this syndrome. We analyzed the components of the ECS in the complete deletion (CD) mouse model of WBS and assessed the impact of its pharmacological modulation in key phenotypes relevant for WBS. CD mice showed the characteristic hypersociable phenotype with no preference for social novelty and poor short-term object-recognition performance. Brain cannabinoid type-1 receptor (CB1R) in CD male mice showed alterations in density and coupling with no detectable change in main endocannabinoids. Endocannabinoid signaling modulation with subchronic (10 days) JZL184, a selective inhibitor of monoacylglycerol lipase, specifically normalized the social and cognitive phenotype of CD mice. Notably, JZL184 treatment improved cardiovascular function and restored gene expression patterns in cardiac tissue. These results reveal the modulation of the ECS as a promising novel therapeutic approach to improve key phenotypic alterations in WBS. Williams-Beuren syndrome (WBS) is a rare disorder that causes hyper-social behavior, intellectual disability, memory problems, and life-threatening overgrowth of the heart. Behavioral therapies can help improve the cognitive and social aspects of the syndrome and surgery is sometimes used to treat the effects on the heart, although often with limited success. However, there are currently no medications available to treat WBS. The endocannabinoid system – which consists of cannabis-like chemical messengers that bind to specific cannabinoid receptor proteins – has been shown to influence cognitive and social behaviors, as well as certain functions of the heart. This has led scientists to suspect that the endocannabinoid system may play a role in WBS, and drugs modifying this network of chemical messengers could help treat the rare condition. To investigate, Navarro-Romero, Galera-López et al. studied mice which had the same genetic deletion found in patients with WBS. Similar to humans, the male mice displayed hyper-social behaviors, had memory deficits and enlarged hearts. Navarro-Romero, Galera-López et al. found that these mutant mice also had differences in the function of the receptor protein cannabinoid type-1 (CB1). The genetically modified mice were then treated with an experimental drug called JZL184 that blocks the breakdown of endocannabinoids which bind to the CB1 receptor . This normalized the number and function of receptors in the brains of the WBS mice, and reduced their social and memory symptoms. The treatment also restored the animals’ heart cells to a more normal size, improved the function of their heart tissue, and led to lower blood pressure. Further experiments revealed that the drug caused the mutant mice to activate many genes in their heart muscle cells to the same level as normal, healthy mice . These findings suggest that JZL184 or other drugs targeting the endocannabinoid system may help ease the symptoms associated with WBS. More studies are needed to test the drug’s effectiveness in humans with this syndrome. Furthermore, the dramatic effect JZL184 has on the heart suggests that it might also help treat high blood pressure or conditions that cause the overgrowth of heart cells.

ENA transporters are a group of P-type ATPases that are characterized by actively moving Na+ or K+ out of the cell against their concentration gradient. The existence of these transporters was initially attributed to some fungi, although more recently they have also been identified in mosses, liverworts, and some protozoa. Given the current increase in the number of organisms whose genomes are completely sequenced, we set out to expand our knowledge about the existence of ENA in organisms belonging to other phylogenetic groups. For that, a hidden Markov model profile was constructed to identify homologous sequences to ENA proteins in protein databases. This analysis allowed us to identify the existence of ENA-type ATPases in the most primitive groups of fungi, as well as in other eukaryotic organisms not described so far. In addition, this study has allowed the identification of a possible new group of P-ATPases, initially proposed as ENA but which maintain phylogenetic distances with these proteins. Finally, this work has also addressed this study of the structure of ENA proteins, which remained unknown due to the lack of crystallographic data. For this purpose, a 3D structure prediction of the NcENA1 protein of the fungus Neurospora crassa was performed using AlphaFold2 software v2.3.1. From this structure, the electrostatic potential of the protein was analyzed. With all these data, the protein regions and the amino acids involved in the transport of Na+ or K+ ions across the membrane were proposed for the first time. Targeted mutagenesis of some of these residues has confirmed their relevant participation in the transport function of ENA proteins.

MAIN CONCLUSION : Arabidopsis plants in NaCl suffering half growth inhibition do not suffer osmotic stress and seldom shoot Na ⁺ toxicity; overaccumulation of Na ⁺ plus K ⁺ might trigger the inhibition. It is widely assumed that salinity inhibits plant growth by osmotic stress and shoot Na⁺ toxicity. This study aims to examine the growth inhibition of Arabidopsis thaliana by NaCl concentrations that allow the completion of the life cycle. Unaffected Col-0 wild-type plants were used to define nontoxic Na⁺ contents; Na⁺ toxicities in shoots and roots were analyzed in hkt1 and sos1 mutants, respectively. The growth inhibition of Col-0 plants at 40 mM Na⁺ was mild and equivalent to that produced by 8 and 4 mM Na⁺ in hkt1 and sos1 plants, respectively. Therefore, these mutants allowed to study the toxicity of Na⁺ in the absence of an osmotic challenge. Col-0 and Ts-1 accessions showed very different Na⁺ contents but similar growth inhibitions; Ts-1 plants showed very high leaf Na⁺ contents but no symptoms of Na⁺ toxicity. Ak-1, C24, and Fei-0 plants were highly affected by NaCl showing evident symptoms of shoot Na⁺ toxicity. Increasing K⁺ in isotonic NaCl/KCl combinations dramatically decreased the Na⁺ content in all Arabidopsis accessions and eliminated the signs of Na⁺ toxicity in most of them but did not relieve growth inhibition. This suggested that the dominant inhibition in these conditions was either osmotic or of an ionic nature unspecific for Na⁺ or K⁺. Col-0 and Ts-1 plants growing in sorbitol showed a clear osmotic stress characterized by a notable decrease of their water content, but this response did not occur in NaCl. Overaccumulation of Na⁺ plus K⁺ might trigger growth reduction in NaCl-treated plants.

Global climate change exacerbates abiotic stresses, as drought, heat, and salt stresses are anticipated to increase significantly in the coming years. Plants coexist with a diverse range of microorganisms. Multiple inter-organismic relationships are known to confer benefits to plants, including growth promotion and enhanced tolerance to abiotic stresses. In this study, we investigated the mutualistic interactions between three fungal endophytes originally isolated from distinct arid environments and an agronomically relevant crop, Solanum lycopersicum . We demonstrated a significant increase in shoot biomass under drought conditions in co-cultivation with Penicillium chrysogenum isolated from Antarctica, Penicillium minioluteum isolated from the Atacama Desert, Chile, and Serendipita indica isolated from the Thar Desert, India. To elucidate plant gene modules commonly induced by the different endophytes that could explain the observed drought tolerance effect in tomato, a comprehensive transcriptomics analysis was conducted. This analysis led to the identification of a shared gene module in the fungus-infected tomato plants. Within this module, gene network analysis enabled us to identify genes related to abscisic acid (ABA) signaling, ABA transport, auxin signaling, ion homeostasis, proline biosynthesis, and jasmonic acid signaling, providing insights into the molecular basis of drought tolerance commonly mediated by fungal endophytes. Our findings highlight a conserved response in the mutualistic interactions between endophytic fungi isolated from unrelated environments and tomato roots, resulting in improved shoot biomass production under drought stress. Key message Despite their genetic and evolutionary distance, two fungal endophytes from the Thar Desert in India, Serendipita indica , and Antarctica, Penicillium chrysogenum , trigger a common transcriptional response in tomato plants to confer increased drought tolerance.

Cardiovascular diseases are the leading cause of death worldwide. Changes in lifestyle and/or pharmacological treatment are able to reduce the burden of coronary artery diseases (CAD) and early diagnosis is crucial for the timely and optimal management of the disease. Stress testing is a good method to measure the burden of CAD but it is time consuming and pharmacological testing may not fully mimic exercise test. The objectives of the present project were to characterize the metabolic profile of the population undergoing pharmacological and exercise stress testing to evaluate possible differences between them, and to assess the capacity of 1 H NMR spectroscopy to predict positive stress testing. Pattern recognition was applied to 1 H NMR spectra from serum of patients undergoing stress test and metabolites were quantified. The effects of the stress test, confounding variables and the ability to predict ischemia were evaluated using OPLS-DA. There was an increase in lactate and alanine concentrations in post-test samples in patients undergoing exercise test, but not in those submitted to pharmacological testing. However, when considering only pharmacological patients, those with a positive test result, showed increased serum lactate, that was masked by the much larger amount of lactate associated to exercise testing. In conclusion, we have established that pharmacological stress test does not reproduce the dynamic changes observed in exercise stress. Although there is promising evidence suggesting that 1 H NMR based metabolomics could predict stress test results, further studies with much larger populations will be required in order to obtain a definitive answer.

Treatments with sodium–glucose 2 cotransporter inhibitors (SGLT2i) or endothelin receptor antagonists (ERA) have shown cardiorenal protective effects. The present study aimed to evaluate the cardiorenal beneficial effects of the combination of SGLT2i and ERA on top of renin–angiotensin system (RAS) blockade. Type 2 diabetic mice (db/db) were treated with different combinations of an SGLT2i (empagliflozin), an ERA (atrasentan), and an angiotensin-converting enzyme inhibitor (ramipril) for 8 weeks. Vehicle-treated diabetic mice and non-diabetic mice were included as controls. Weight, blood glucose, blood pressure, and kidney and heart function were monitored during the study. Kidneys and heart were collected for histological examination and to study the intrarenal RAS. Treatment with empagliflozin alone or combined significantly decreased blood glucose compared to vehicle-treated db/db. The dual and triple therapies achieved significantly greater reductions in diastolic blood pressure than ramipril alone. Compared to vehicle-treated db/db, empagliflozin combined with ramipril or in triple therapy significantly prevented GFR increase, but only the triple combination exerted greater protection against podocyte loss. In the heart, empagliflozin alone or combined reduced cardiac isovolumetric relaxation time (IVRT) and left atrium (LA) diameter as compared to vehicle-treated db/db. However, only the triple therapy was able to reduce cardiomyocyte area. Importantly, the add-on triple therapy further enhanced the intrarenal ACE2/Ang(1-7)/Mas protective arm of the RAS. These data suggest that triple therapy with empagliflozin, atrasentan and ramipril show synergistic cardiorenal protective effects in a type 2 diabetic mouse model.

Heart failure (HF) impairs diaphragm function. Animal models realistically mimicking HF should feature both the cardiac alterations and the diaphragmatic dysfunction characterizing this disease. The isoproterenol-induced HF model is widely used, but whether it presents diaphragmatic dysfunction is unknown. However, indirect data from research in other fields suggest that isoproterenol could increase diaphragm function. The aim of this study was to test the hypothesis that the widespread rodent model of isoproterenol-induced HF results in increased diaphragmatic contractility. Forty C57BL/6J male mice were randomized into 2 groups: HF and healthy controls. After 30 days of isoproterenol infusion to establish HF, in vivo diaphragmatic excursion and ex vivo isolated diaphragm contractibility were measured. As compared with healthy controls, mice with isoproterenol-induced HF showed the expected changes in structural and functional echocardiographic parameters and lung edema. isoproterenol-induced HF increased in vivo diaphragm excursion (by ≈30%, p<0.01) and increased by ≈50% both ex vivo peak specific force (p<0.05) and tetanic force (p<0.05) at almost all 10–100 Hz frequencies (p<0.05), with reduced fatigue resistance (p<0.01) when compared with healthy controls. Expression of myosin genes encoding the main muscle fiber types revealed that Myh4 was higher in isoproterenol-induced HF than in healthy controls (p<0.05), suggesting greater distribution of type IIb fibers. These results show that the conventional isoproterenol-induced HF model increases diaphragm contraction, a finding contrary to what is observed in patients with HF. Therefore, this specific model seems limited for translational an integrative HF research, especially when cardio-respiratory interactions are investigated.