Explore the vast range of titles available.

High concentrations of sodium (Na+), chloride (Cl−), calcium (Ca2+), and sulphate (SO42−) are frequently found in saline soils. Crop plants cannot successfully develop and produce because salt stress impairs the uptake of Ca2+, potassium (K+), and water into plant cells. Different intracellular and extracellular ionic concentrations change with salinity, including those of Ca2+, K+, and protons. These cations serve as stress signaling molecules in addition to being essential for ionic homeostasis and nutrition. Maintaining an appropriate K+:Na+ ratio is one crucial plant mechanism for salt tolerance, which is a complicated trait. Another important mechanism is the ability for fast extrusion of Na+ from the cytosol. Ca2+ is established as a ubiquitous secondary messenger, which transmits various stress signals into metabolic alterations that cause adaptive responses. When plants are under stress, the cytosolic-free Ca2+ concentration can rise to 10 times or more from its resting level of 50–100 nanomolar. Reactive oxygen species (ROS) are linked to the Ca2+ alterations and are produced by stress. Depending on the type, frequency, and intensity of the stress, the cytosolic Ca2+ signals oscillate, are transient, or persist for a longer period and exhibit specific “signatures”. Both the influx and efflux of Ca2+ affect the length and amplitude of the signal. According to several reports, under stress Ca2+ alterations can occur not only in the cytoplasm of the cell but also in the cell walls, nucleus, and other cell organelles and the Ca2+ waves propagate through the whole plant. Here, we will focus on how wheat and other important crops absorb Na+, K+, and Cl− when plants are under salt stress, as well as how Ca2+, K+, and pH cause intracellular signaling and homeostasis. Similar mechanisms in the model plant Arabidopsis will also be considered. Knowledge of these processes is important for understanding how plants react to salinity stress and for the development of tolerant crops.

Here, the effects of the ethylene-releasing compound, ethephon, and the ethylene precursor, 1-aminocyclopropane-1-carboxylic acid (ACC), on ionic currents across plasma membranes and on the cytosolic Ca²⁺ activity ([Ca²⁺]c) of tobacco (Nicotiana tabacum) suspension cells were characterized using a patch-clamp technique and confocal laser scanning microscopy. Exposure of tobacco protoplasts to ethephon and ACC led to activation of a plasma membrane cation channel that was permeable to Ba²⁺, Mg²⁺ and Ca²⁺, and inhibited by La³⁺, Gd³⁺ and Al³⁺. The ethephon- and ACC-induced Ca²⁺-permeable channel was abolished by the antagonist of ethylene perception (1-metycyclopropene) and by the inhibitor of ACC synthase (aminovinylglycin), indicating that activation of the Ca²⁺-permeable channels results from ethylene. Ethephon elicited an increase in the [Ca²⁺]c of tobacco suspension cells, as visualized by the Ca²⁺-sensitive probe Fluo-3 and confocal microscopy. The ethephon-induced elevation of [Ca²⁺]c was markedly inhibited by Gd³⁺ and BAPTA, suggesting that an influx of Ca²⁺ underlies the elevation of [Ca²⁺]c. These results indicate that an elevation of [Ca²⁺]c, resulting from activation of the plasma membrane Ca²⁺-permeable channels by ethylene, is an essential component in ethylene signaling in plants.

During drought, abscisic acid (ABA) induces closure of stomata via a signaling pathway that involves the calcium (Ca2+)-independent protein kinase OST1, as well as Ca2+-dependent protein kinases. However, the interconnection between OST1 and Ca2+ signaling in ABA-induced stomatal closure has not been fully resolved. ABA-induced Ca2+ signals were monitored in intact Arabidopsis leaves, which express the ratiometric Ca2+ reporter R-GECO1-mTurquoise and the Ca2+-dependent activation of S-type anion channels was recorded with intracellular double-barreled microelectrodes. ABA triggered Ca2+ signals that occurred during the initiation period, as well as in the acceleration phase of stomatal closure. However, a subset of stomata closed in the absence of Ca2+ signals. On average, stomata closed faster if Ca2+ signals were elicited during the ABA response. Loss of OST1 prevented ABA-induced stomatal closure and repressed Ca2+ signals, whereas elevation of the cytosolic Ca2+ concentration caused a rapid activation of SLAC1 and SLAH3 anion channels. Our data show that the majority of Ca2+ signals are evoked during the acceleration phase of stomatal closure, which is initiated by OST1. These Ca2+ signals are likely to activate Ca2+-dependent protein kinases, which enhance the activity of S-type anion channels and boost stomatal closure.

• Cytosolic calcium signals are evoked by a large variety of biotic and abiotic stimuli and play an important role in cellular and long distance signalling in plants. While the function of the plasma membrane in cytosolic Ca2+ signalling has been intensively studied, the role of the vacuolar membrane remains elusive. • A newly developed vacuolar voltage clamp technique was used in combination with live-cell imaging, to study the role of the vacuolar membrane in Ca2+ and pH homeostasis of bulging root hair cells of Arabidopsis. • Depolarisation of the vacuolar membrane caused a rapid increase in the Ca2+ concentration and alkalised the cytosol, while hyperpolarisation led to the opposite responses. • The relationship between the vacuolar membrane potential, the cytosolic pH and Ca2+ concentration suggests that a vacuolar H⁺/Ca2+ exchange mechanism plays a central role in cytosolic Ca2+ homeostasis. Mathematical modelling further suggests that the voltage-dependent vacuolar Ca2+ homeostat could contribute to calcium signalling when coupled to a recently discovered K⁺ channel-dependent module for electrical excitability of the vacuolar membrane.

Calcium is an essential plant nutrient. It is required for various structural roles in the cell wall and membranes, it is a counter‐cation for inorganic and organic anions in the vacuole, and the cytosolic Ca2+ concentration ([Ca2+]cyt) is an obligate intracellular messenger coordinating responses to numerous developmental cues and environmental challenges. This article provides an overview of the nutritional requirements of different plants for Ca, and how this impacts on natural flora and the Ca content of crops. It also reviews recent work on (a) the mechanisms of Ca2+ transport across cellular membranes, (b) understanding the origins and specificity of [Ca2+]cyt signals and (c) characterizing the cellular [Ca2+]cyt‐sensors (such as calmodulin, calcineurin B‐like proteins and calcium‐dependent protein kinases) that allow plant cells to respond appropriately to [Ca2+]cyt signals.

Stomata are crucial structures in plants that play a primary role in the infection process during a pathogen’s attack, as they act as points of access for invading pathogens to enter host tissues. Recent evidence has revealed that stomata are integral to the plant defense system and can actively impede invading pathogens by triggering plant defense responses. Stomata interact with diverse pathogen virulence factors, granting them the capacity to influence plant susceptibility and resistance. Moreover, recent studies focusing on the environmental and microbial regulation of stomatal closure and opening have shed light on the epidemiology of bacterial diseases in plants. Bacteria and fungi can induce stomatal closure using pathogen-associated molecular patterns (PAMPs), effectively preventing entry through these openings and positioning stomata as a critical component of the plant’s innate immune system; however, despite this defense mechanism, some microorganisms have evolved strategies to overcome stomatal protection. Interestingly, recent research supports the hypothesis that stomatal closure caused by PAMPs may function as a more robust barrier against pathogen infection than previously believed. On the other hand, plant stomatal closure is also regulated by factors such as abscisic acid and Ca2+-permeable channels, which will also be discussed in this review. Therefore, this review aims to discuss various roles of stomata during biotic and abiotic stress, such as insects and water stress, and with specific context to pathogens and their strategies for evading stomatal defense, subverting plant resistance, and overcoming challenges faced by infectious propagules. These pathogens must navigate specific plant tissues and counteract various constitutive and inducible resistance mechanisms, making the role of stomata in plant defense an essential area of study.

The Ca 2+ -selective transient receptor potential vanilloid 6 (TRPV6) channel plays a fundamental role in the female and male murine reproductive system. We have previously shown that TRPV6 is essential for male fertility, and necessary for a proper placental Ca 2+ transport, embryonic bone development and calcification, as well as for extracellular matrix formation in the placental labyrinth. Here, we show that lack of functional TRPV6 results in impaired fecundity in female mice with increased latency to first pregnancy, longer interpregnancy intervals and fewer and smaller litters. In mouse endometrium the TRPV6 protein is expressed in epithelial cells (MEECs). Using patch clamp recording and Ca 2+ imaging, we show TRPV6-dependent whole-cell currents and that TRPV6 contributes to cytoplasmic Ca 2+ signaling in MEECs. MEECs lacking functional TRPV6 Ca 2+ channels reveal a significantly reduced frequency of spontaneous cytosolic Ca 2+ oscillations, shown in isolated cells and in situ in whole mount uterus preparations. Our results reveal a previously unknown physiological role for TRPV6 in the regulation of endometrial Ca 2+ homeostasis and its impact on female fecundity in mice, providing a molecular and cellular framework for further investigation of reproductive disorders, such as those associated with defective Ca 2+ regulation in women.

Mitogen‐activated protein kinases (MPKs) play critical roles in signalling and growth, and Ca²⁺and H₂O₂control plant growth processes associated with abscisic acid (ABA). However, it remains unclear how MPKs are involved in H₂O₂‐ and Ca²⁺‐mediated root elongation. Root elongation in seedlings of the loss‐of‐function mutant Atmpk6 (Arabidopsis thaliana MPK6) was less sensitive to moderate H₂O₂or ABA than that in wild‐type (WT) plants. The enhanced elongation was a result of root cell expansion. This effect disappeared when ABA‐induced H₂O₂accumulation or the cytosolic Ca²⁺increase were defective. Molecular and biochemical evidence showed that increased expression of the cell wall peroxidase PRX34 in Atmpk6 root cells enhanced apoplastic H₂O₂generation; this promoted a cytosolic Ca²⁺increase and Ca²⁺influx across the plasma membrane. The plasma membrane damage caused by high levels of H₂O₂was ameliorated in a Ca²⁺‐dependent manner. These results suggested that there was intensified PRX34‐mediated H₂O₂generation in the apoplast and increased Ca²⁺flux into the cytosol of Atmpk6 root cells; that is, the spatial separation of apoplastic H₂O₂from cytosolic Ca²⁺in root cells prevented H₂O₂‐induced inhibition of root elongation in Atmpk6 seedlings.

Enhancement of the late sodium current (INaL) increases arrhythmia propensity in the heart, whereas suppression of the current is antiarrhythmic. In the present study, we investigated INaL in canine ventricular cardiomyocytes under action potential voltage-clamp conditions using the selective Na+ channel inhibitors GS967 and tetrodotoxin. Both 1 µM GS967 and 10 µM tetrodotoxin dissected largely similar inward currents. The amplitude and integral of the GS967-sensitive current was significantly smaller after the reduction of intracellular Ca2+ concentration ([Ca2+]i) either by superfusion of the cells with 1 µM nisoldipine or by intracellular application of 10 mM BAPTA. Inhibiting calcium/calmodulin-dependent protein kinase II (CaMKII) by KN-93 or the autocamtide-2-related inhibitor peptide similarly reduced the amplitude and integral of INaL. Action potential duration was shortened in a reverse rate-dependent manner and the plateau potential was depressed by GS967. This GS967-induced depression of plateau was reduced by pretreatment of the cells with BAPTA-AM. We conclude that (1) INaL depends on the magnitude of [Ca2+]i in canine ventricular cells, (2) this [Ca2+]i-dependence of INaL is mediated by the Ca2+-dependent activation of CaMKII, and (3) INaL is augmented by the baseline CaMKII activity.

d-allulose, a rare sugar, has sweetness with few calories. d-allulose regulates feeding and glycemia, and ameliorates hyperphagia, obesity and diabetes. All these functions involve the central nervous system. However, central mechanisms underlying these effects of d-allulose remain unknown. We recently reported that d-allulose activates the anorexigenic neurons in the hypothalamic arcuate nucleus (ARC), the neurons that respond to glucagon-like peptide-1 and that express proopiomelanocortin. However, its action on the orexigenic neurons remains unknown. This study investigated the effects of d-allulose on the ARC neurons implicated in hunger, by measuring cytosolic Ca2+ concentration ([Ca2+]i) in single neurons. d-allulose depressed the increases in [Ca2+]i induced by ghrelin and by low glucose in ARC neurons and inhibited spontaneous oscillatory [Ca2+]i increases in neuropeptide Y (NPY) neurons. d-allulose inhibited 10 of 35 (28%) ghrelin-responsive, 18 of 60 (30%) glucose-sensitive and 3 of 8 (37.5%) NPY neurons in ARC. Intracerebroventricular injection of d-allulose inhibited food intake at 20:00 and 22:00, the early dark phase when hunger is promoted. These results indicate that d-allulose suppresses hunger-associated feeding and inhibits hunger-promoting neurons in ARC. These central actions of d-allulose represent the potential of d-allulose to inhibit the hyperphagia with excessive appetite, thereby counteracting obesity and diabetes.