Spatiotemporal Calcium Research Articles

Generalised Neuronal Calcium Dynamics of Membrane and ER in the Polar Dimension.

Calcium ions are the second messenger playing as regulators for various cellular activities. Its spatiotemporal control is critical for various brain functions, including neuroplasticity, apoptosis, and cell death. The Endoplasmic Reticulum (ER) plays an important role in determining these spatiotemporal calcium dynamics. Stromal interaction molecule (STIM) - Orai channel on the membrane generates additional calcium flow, whereas other membrane fluxes contribute to cytosolic flux. Due to their anomalous character, we used the Caputo fractional differential operator to mimic these interactions in polar coordinates. Solutions were generated using hybrid integral transform methods to control the analytical approach. Using Green's function yielded a closed-form solution for Mittag-Leffler-type functions. This work emphasizes the significant relationship between calcium and various buffer levels in neurons. The differential transition simulation of a time derivative with space across different parameters indicated a decrease in calcium concentration. Anomalously low buffer levels exhibited the impact of Alzheimer's disease on calcium higher concentration, leading to the death of neurons. Additionally, the research introduces a method involving S100B, BAPTA, and calmodulin buffers to uphold optimal calcium levels within the neuronal cytosol. The applicability of this model with different buffer properties and parameters and memory impacts the calcium concentration with the neurological disorder.

Regulatory disturbances in the dynamical signaling systems of and NO in fibroblasts cause fibrotic disorders.

Studying the calcium dynamics within a fibroblast cell individually has provided only a restricted understanding of its functions. However, research efforts focusing on systems biology approaches for such investigations have been largely neglected by researchers until now. Fibroblast cells rely on signaling from calcium and nitric oxide (NO) to maintain their physiological functions and structural stability. Various studies have demonstrated the correlation between NO and the control of dynamics in cells. However, there is currently no existing model to assess the disruptions caused by various factors in regulatory dynamics, potentially resulting in diverse fibrotic disorders. A mathematical model has been developed to investigate the effects of changes in parameters such as buffer, receptor, sarcoplasmic endoplasmic reticulum -ATPase (SERCA) pump, and source influx on the regulation and dysregulation of spatiotemporal calcium and NO dynamics in fibroblast cells. This model is based on a system of reaction-diffusion equations, and numerical simulations are conducted using the finite element method. Disturbances in key processes related to calcium and nitric oxide, including source influx, buffer mechanism, SERCA pump, and inositol trisphosphate receptor, may contribute to deregulation in the calcium and NO dynamics within fibroblasts. The findings also provide new insights into the extent and severity of disorders resulting from alterations in various parameters, potentially leading to deregulation and the development of fibrotic disease.

Simulation of biochemical dynamics of [Formula: see text] and [Formula: see text] in fibroblast cell.

Calcium dynamics is not only responsible for maintaining the framework and functions of the cell but also plays a role in the dynamics of other biochemical systems in the cell. Phospholipase C-[Formula: see text] l ([Formula: see text]) has a crucial role in the function of fibroblast cells. Experiments have shown that [Formula: see text] and [Formula: see text] have interdependent dynamics in fibroblast cells. However, no reaction-diffusion model exists for the two-way feedback system dynamics of [Formula: see text] and [Formula: see text] in fibroblasts till date. The computational model is designed to investigate the impact of variations in several processes, such as the [Formula: see text] pump, buffer process, source inflow, etc., on the system dynamics of [Formula: see text] and [Formula: see text] in fibroblast cells. The computational findings are obtained using finite element techniques, and the consequences of dysregulation in various processes on the spatiotemporal calcium and [Formula: see text] dynamics in fibroblasts are investigated. The results lead to the conclusion that the effects of buffer, source influx, diffusion, and [Formula: see text] pump can cause fluctuations in the dynamics of [Formula: see text] and [Formula: see text] in fibroblasts. Disruptions in these constitutive processes can result in changes in the dynamics of calcium and [Formula: see text]. Thus, the current model provides new/novel information regarding the precise dysregulatory constitutive systems that regulate calcium and [Formula: see text] kinetics, such as source inflow, diffusion, [Formula: see text], and buffer, can be responsible for excessive calcium and [Formula: see text] concentrations leading to fibrotic illnesses such as cancer and fibrosis.

Fractional order reaction diffusion of calcium regulating NFAT production in T Lymphocyte

[Formula: see text] signals have a crucial role in the immune system for cell functions such as proliferation, differentiation, apoptosis and gene transcription as well as the activation of Nuclear factor of activated T Cell (NFAT) which modulates the immune response of the cells. In this study, a fractional order spatiotemporal calcium dynamics model is formulated using the reaction-diffusion equation incorporating parameters like buffers, source influx, [Formula: see text] and [Formula: see text]. Grünwald estimation is employed to obtain the solution and stability analysis has been performed. The analysis of numerical results provides novel insights about the role of Brownian motion, super diffusion, source influx, buffers, etc., in the regulation of calcium and NFAT concentration levels in T cell and the conditions which might lead to disordered immune responses causing diseases such as HINI, HIV and HBV.

Timescale of hole closure during plasma membrane repair estimated by calcium imaging and numerical modeling

Plasma membrane repair is essential for eukaryotic cell life and is triggered by the influx of calcium through membrane wounds. Repair consists of sequential steps, with closure of the membrane hole being the key event that allows the cell to recover, thus identifying the kinetics of hole closure as important for clarifying repair mechanisms and as a quantitative handle on repair efficiency. We implement calcium imaging in MCF7 breast carcinoma cells subject to laser damage, coupled with a model describing the spatio-temporal calcium distribution. The model identifies the time point of hole closure as the time of maximum calcium signal. Analysis of cell data estimates the closure time as: langle t_c rangle =5.45pm 2.25 s and langle t_c rangle =6.81pm 4.69 s using GCaMP6s-CAAX and GCaMP6s probes respectively. The timescale was confirmed by independent time-lapse imaging of a hole during sealing. Moreover, the analysis estimates the characteristic time scale of calcium removal, the penetration depth of the calcium wave and the diffusion coefficient. Probing of hole closure times emerges as a strong universal tool for quantification of plasma membrane repair

Measuring nuclear calcium and actin assembly in living cells.

Nuclear calcium signalling has emerged as a critical mechanism regulating processes like chromatin organization and gene expression. Recently, we have shown that nuclear calcium elevation triggers rapid and transient actin filament assembly inside the nucleus. Here, we constructed and employed a nuclear-specific calcium sensor based upon the new generation of genetically encoded probes jGCaMP7f. By fusing a nuclear localization signal to jGCaMP7f, we achieved highly efficient nuclear-specific targeting. Comparing the jGCaMP7f-NLS probe with the previous GCaMP6f-NLS calcium sensor showed clearly that jGCaMP7f-NLS is more sensitive and reverses significantly quicker thereby reflecting rapid nuclear calcium transients in a closely physiological manner. We further confirm that nuclear calcium transients precede nuclear actin polymerization by several seconds. Our data show that calcium-triggered nuclear actin assembly in fibroblasts is independent of the actin nucleating Arp2/3 complex. Together, jGCaMP7f-NLS represents an easy to use, reliable and highly sensitive nuclear calcium sensor that allows to tightly interrogate real-time, spatiotemporal calcium signalling and calcium-elicited effects in the nucleus of living cells.

In vivo microstimulation with cathodic and anodic asymmetric waveforms modulates spatiotemporal calcium dynamics in cortical neuropil and pyramidal neurons of male mice.

Electrical stimulation has been critical in the development of an understanding of brain function and disease. Despite its widespread use and obvious clinical potential, the mechanisms governing stimulation in the cortex remain largely unexplored in the context of pulse parameters. Modeling studies have suggested that modulation of stimulation pulse waveform may be able to control the probability of neuronal activation to selectively stimulate either cell bodies or passing fibers depending on the leading polarity. Thus, asymmetric waveforms with equal charge per phase (i.e., increasing the leading phase duration and proportionately decreasing the amplitude) may be able to activate a more spatially localized or distributed population of neurons if the leading phase is cathodic or anodic, respectively. Here, we use two-photon and mesoscale calcium imaging of GCaMP6s expressed in excitatory pyramidal neurons of male mice to investigate the role of pulse polarity and waveform asymmetry on the spatiotemporal properties of direct neuronal activation with 10-Hz electrical stimulation. We demonstrate that increasing cathodic asymmetry effectively reduces neuronal activation and results in a more spatially localized subpopulation of activated neurons without sacrificing the density of activated neurons around the electrode. Conversely, increasing anodic asymmetry increases the spatial spread of activation and highly resembles spatiotemporal calcium activity induced by conventional symmetric cathodic stimulation. These results suggest that stimulation polarity and asymmetry can be used to modulate the spatiotemporal dynamics of neuronal activity thus increasing the effective parameter space of electrical stimulation to restore sensation and study circuit dynamics.

Arrhythmia mechanisms and spontaneous calcium release: Bi-directional coupling between re-entrant and focal excitation.

Spontaneous sub-cellular calcium release events (SCRE) are conjectured to promote rapid arrhythmias associated with conditions such as heart failure and atrial fibrillation: they can underlie the emergence of spontaneous action potentials in single cells which can lead to arrhythmogenic triggers in tissue. The multi-scale mechanisms of the development of SCRE into arrhythmia triggers, and their dynamic interaction with the tissue substrate, remain elusive; rigorous and simultaneous study of dynamics from the nanometre to the centimetre scale is a major challenge. The aim of this study was to develop a computational approach to overcome this challenge and study potential bi-directional coupling between sub-cellular and tissue-scale arrhythmia phenomena. A framework comprising a hierarchy of computational models was developed, which includes detailed single-cell models describing spatio-temporal calcium dynamics in 3D, efficient non-spatial cell models, and both idealised and realistic tissue models. A phenomenological approach was implemented to reproduce SCRE morphology and variability in the efficient cell models, comprising the definition of analytical Spontaneous Release Functions (SRF) whose parameters may be randomly sampled from appropriate distributions in order to match either the 3D cell models or experimental data. Pro-arrhythmogenic pacing protocols were applied to initiate re-entry and promote calcium overload, leading to the emergence of SCRE. The SRF accurately reproduced the dynamics of SCRE and its dependence on environment variables under multiple different conditions. Sustained re-entrant excitation promoted calcium overload, and led to the emergence of focal excitations after termination. A purely functional mechanism of re-entry and focal activity localisation was demonstrated, related to the unexcited spiral wave core. In conclusion, a novel approach has been developed to dynamically model SCRE at the tissue scale, which facilitates novel, detailed multi-scale mechanistic analysis. It was revealed that complex re-entrant excitation patterns and SCRE may be bi-directionally coupled, promoting novel mechanisms of arrhythmia perpetuation.

STIM1 Is Required for Remodeling of the Endoplasmic Reticulum and Microtubule Cytoskeleton in Steering Growth Cones.

The spatial and temporal regulation of calcium signaling in neuronal growth cones is essential for axon guidance. In growth cones, the endoplasmic reticulum (ER) is a significant source of calcium signals. However, it is not clear whether the ER is remodeled during motile events to localize calcium signals in steering growth cones. The expression of the ER-calcium sensor, stromal interacting molecule 1 (STIM1) is necessary for growth cone steering toward the calcium-dependent guidance cue BDNF, with STIM1 functioning to sustain calcium signals through store-operated calcium entry. However, STIM1 is also required for growth cone steering away from semaphorin-3a, a guidance cue that does not activate ER-calcium release, suggesting multiple functions of STIM1 within growth cones (Mitchell et al., 2012). STIM1 also interacts with microtubule plus-end binding proteins EB1/EB3 (Grigoriev et al., 2008). Here, we show that STIM1 associates with EB1/EB3 in growth cones and that STIM1 expression is critical for microtubule recruitment and subsequent ER remodeling to the motile side of steering growth cones. Furthermore, we extend our data in vivo, demonstrating that zSTIM1 is required for axon guidance in actively navigating zebrafish motor neurons, regulating calcium signaling and filopodial formation. These data demonstrate that, in response to multiple guidance cues, STIM1 couples microtubule organization and ER-derived calcium signals, thereby providing a mechanism where STIM1-mediated ER remodeling, particularly in filopodia, regulates spatiotemporal calcium signals during axon guidance.SIGNIFICANCE STATEMENT Defects in both axon guidance and endoplasmic reticulum (ER) function are implicated in a range of developmental disorders. During neuronal circuit development, the spatial localization of calcium signals controls the growth cone cytoskeleton to direct motility. We demonstrate a novel role for stromal interacting molecule 1 (STIM1) in regulating microtubule and subsequent ER remodeling in navigating growth cones. We show that STIM1, an activator of store-operated calcium entry, regulates the dynamics of microtubule-binding proteins EB1/EB3, coupling ER to microtubules, within filopodia, thereby steering growth cones. The STIM1-microtubule-ER interaction provides a new model for spatial localization of calcium signals in navigating growth cones in the nascent nervous system.

Simulation of Buffered Advection Diffusion of Calcium in a Hepatocyte Cell

The calcium signaling is the basic and vital component of cell communication in almost all types of human and animal cells. All the vital functions of parenchymal cell of liver known as hepatocyte cell are regulated by this calcium signaling. The calcium concentration at specific levels are responsible for each of the various functions of the cell. The deeper understanding of the mechanisms and the factors affecting the calcium dynamics in a hepatocyte cell is vital for various clinical applications related to diseases of the liver. In this paper, mathematical model is proposed to study intracellular calcium dynamics in hepatocyte cell by incorporating the processes like diffusion, advection, buffering etc. The reaction advection diffusion equation has been employed for a two dimensional unsteady state case, to form an initial and boundary value problem. The initial and boundary conditions are formulated based on the physical conditions of cell. Finite volume method and Crank Nicolson scheme have been employed along spatial and temporal dimension respectively to obtain numerical solution. The impact of endogenous and exogenous buffers, advection and diffusion on calcium dynamics in hepatocyte cell has been studied with the help of numerical results. The rise and fall in spatio-temporal calcium concentration in hepatocyte cell in response to specific conditions of advection, diffusion and buffer concentrations is observed. These variations in spatio-temporal calcium concentrations are regulated in narrow range due to fine coordination among these processes of cell under normal environmental and physiological conditions. The proposed model gives better understanding of interrelationship and interdependence of these physical processes for fine coordination among them to maintain structure and functions of cell.

Three-Dimensional Finite Element Model to Study Effect of RyR Calcium Channel, ER Leak and SERCA Pump on Calcium Distribution in Oocyte Cell

Calcium ions control many cellular processes by relaying signals in the form of their spatio-temporal distribution. Dynamics and patterns of calcium concentration such as repetitive waves, coherent oscillations or spatially localized elevations activate diverse physiological functions. Calcium is the most universal second messenger in cells and plays an important role in initiation, sustenance and termination of various activities in cells required for maintaining the structure and function of the cell. Calcium signal at fertilization is necessary for egg activation and exhibits specialized spatial and temporal dynamics. The specific calcium concentration distribution patterns in oocytes required for various activities like egg fertilization, maturation, etc. are not well understood. In this paper, a three-dimensional finite element model is proposed to study the spatio-temporal calcium distribution in oocytes. The parameters such as buffers, SERCA pump, ER Leak, ryanodine receptor (RyR) calcium channel, point source and line source of calcium are incorporated in the model. The appropriate initial and boundary conditions have been framed on the basis of the physical condition of the problem. A program is developed in MATLAB for simulation. The results have been used to study the effect of source geometry, RyR calcium channel, ER Leak, SERCA pump and buffers on cytosolic calcium concentration distribution in oocytes.

Calcium Signaling in Liver Injury and Regeneration.

The liver fulfills central roles in metabolic control and detoxification and, as such, is continuously exposed to a plethora of insults. Importantly, the liver has a unique ability to regenerate and can completely recoup from most acute, non-iterative insults. However, multiple conditions, including viral hepatitis, non-alcoholic fatty liver disease (NAFLD), long-term alcohol abuse and chronic use of certain medications, can cause persistent injury in which the regenerative capacity eventually becomes dysfunctional, resulting in hepatic scaring and cirrhosis. Calcium is a versatile secondary messenger that regulates multiple hepatic functions, including lipid and carbohydrate metabolism, as well as bile secretion and choleresis. Accordingly, dysregulation of calcium signaling is a hallmark of both acute and chronic liver diseases. In addition, recent research implicates calcium transients as essential components of liver regeneration. In this review, we provide a comprehensive overview of the role of calcium signaling in liver health and disease and discuss the importance of calcium in the orchestration of the ensuing regenerative response. Furthermore, we highlight similarities and differences in spatiotemporal calcium regulation between liver insults of different etiologies. Finally, we discuss intracellular calcium control as an emerging therapeutic target for liver injury and summarize recent clinical findings of calcium modulation for the treatment of ischemic-reperfusion injury, cholestasis and NAFLD.

Critical and Supercritical Spatiotemporal Calcium Dynamics in Beta Cells.

A coordinated functioning of beta cells within pancreatic islets is mediated by oscillatory membrane depolarization and subsequent changes in cytoplasmic calcium concentration. While gap junctions allow for intraislet information exchange, beta cells within islets form complex syncytia that are intrinsically nonlinear and highly heterogeneous. To study spatiotemporal calcium dynamics within these syncytia, we make use of computational modeling and confocal high-speed functional multicellular imaging. We show that model predictions are in good agreement with experimental data, especially if a high degree of heterogeneity in the intercellular coupling term is assumed. In particular, during the first few minutes after stimulation, the probability distribution of calcium wave sizes is characterized by a power law, thus indicating critical behavior. After this period, the dynamics changes qualitatively such that the number of global intercellular calcium events increases to the point where the behavior becomes supercritical. To better mimic normal in vivo conditions, we compare the described behavior during supraphysiological non-oscillatory stimulation with the behavior during exposure to a slightly lower and oscillatory glucose challenge. In the case of this protocol, we observe only critical behavior in both experiment and model. Our results indicate that the loss of oscillatory changes, along with the rise in plasma glucose observed in diabetes, could be associated with a switch to supercritical calcium dynamics and loss of beta cell functionality.

Impact of spatiotemporal calcium dynamics within presynaptic active zones on synaptic delay at the frog neuromuscular junction.

The spatiotemporal calcium dynamics within presynaptic neurotransmitter release sites (active zones, AZs) at the time of synaptic vesicle fusion is critical for shaping the dynamics of neurotransmitter release. Specifically, the relative arrangement and density of voltage-gated calcium channels (VGCCs) as well as the concentration of calcium buffering proteins can play a large role in the timing, magnitude, and plasticity of release by shaping the AZ calcium profile. However, a high-resolution understanding of the role of AZ structure in spatiotemporal calcium dynamics and how it may contribute to functional heterogeneity at an adult synapse is currently lacking. We demonstrate that synaptic delay varies considerably across, but not within, individual synapses at the frog neuromuscular junction (NMJ). To determine how elements of the AZ could contribute to this variability, we performed a parameter search using a spatially realistic diffusion reaction-based computational model of a frog NMJ AZ (Dittrich M, Pattillo JM, King JD, Cho S, Stiles JR, Meriney SD. Biophys J 104: 2751-2763, 2013; Ma J, Kelly L, Ingram J, Price TJ, Meriney SD, Dittrich M. J Neurophysiol 113: 71-87, 2015). We demonstrate with our model that synaptic delay is sensitive to significant alterations in the spatiotemporal calcium dynamics within an AZ at the time of release caused by manipulations of the density and organization of VGCCs or by the concentration of calcium buffering proteins. Furthermore, our data provide a framework for understanding how AZ organization and structure are important for understanding presynaptic function and plasticity. NEW & NOTEWORTHY The structure of presynaptic active zones (AZs) can play a large role in determining the dynamics of neurotransmitter release across many model preparations by influencing the spatiotemporal calcium dynamics within the AZ at the time of vesicle fusion. However, less is known about how different AZ structural schemes may influence the timing of neurotransmitter release. We demonstrate that variations in AZ structure create different spatiotemporal calcium profiles that, in turn, lead to differences in synaptic delay.

Three-dimensional finite element model to study calcium distribution in oocytes

Calcium is the most universal second messenger in cells and plays an important role in initiation, sustenance and termination of various activities in cells required for maintaining the structure and function of the cell. Calcium signal at fertilization is necessary for egg activation and exhibits specialized spatial and temporal dynamics. The specific calcium concentration distribution patterns in oocytes required for various activities such as egg fertilization and maturation are not well understood. In this paper, a three-dimensional finite element model is proposed to study the spatio-temporal calcium distribution in oocyte. The parameters such as buffers, SERCA pump, RyR calcium channel, point source and line source of calcium are incorporated in the model. The appropriate initial and boundary conditions have been framed on the basis of physical condition of the problem. A program is developed in MATLAB for simulation. The results have been used to study the effect of source geometry, RyR calcium channel, SERCA pump and buffers on cytosolic calcium concentration distribution in oocyte.

Calcium spikes, waves and oscillations in a large, patterned epithelial tissue

While calcium signaling in excitable cells, such as muscle or neurons, is extensively characterized, calcium signaling in epithelial tissues is little understood. Specifically, the range of intercellular calcium signaling patterns elicited by tightly coupled epithelial cells and their function in the regulation of epithelial characteristics are little explored. We found that in Drosophila imaginal discs, a widely studied epithelial model organ, complex spatiotemporal calcium dynamics occur. We describe patterns that include intercellular waves traversing large tissue domains in striking oscillatory patterns as well as spikes confined to local domains of neighboring cells. The spatiotemporal characteristics of intercellular waves and oscillations arise as emergent properties of calcium mobilization within a sheet of gap-junction coupled cells and are influenced by cell size and environmental history. While the in vivo function of spikes, waves and oscillations requires further characterization, our genetic experiments suggest that core calcium signaling components guide actomyosin organization. Our study thus suggests a possible role for calcium signaling in epithelia but importantly, introduces a model epithelium enabling the dissection of cellular mechanisms supporting the initiation, transmission and regeneration of long-range intercellular calcium waves and the emergence of oscillations in a highly coupled multicellular sheet.

Nuclear pores enable sustained perinuclear calcium oscillations.

BackgroundCalcium signalling relies on the flux of calcium ions across membranes yet how signals in different compartments are related remains unclear. In particular, similar calcium signals on both sides of the nuclear envelope have been reported and attributed to passive diffusion through nuclear pores. However, observed differing cytosolic and nucleosolic calcium signatures suggest that the signalling machinery in these compartments can act independently.ResultsWe adapt the fire-diffuse-fire model to investigate the generation of perinuclear calcium oscillations. We demonstrate that autonomous spatio-temporal calcium patterns are still possible in the presence of nuclear and cytosolic coupling via nuclear pores. The presence or absence of this autonomy is dependent upon the strength of the coupling and the maximum firing rate of an individual calcium channel. In all cases, coupling through the nuclear pores enables robust signalling with respect to changes in the diffusion constant.ConclusionsWe show that contradictory interpretations of experimental data with respect to the autonomy of nuclear calcium oscillations can be reconciled within one model, with different observations being a consequence of varying nuclear pore permeabilities for calcium and refractory conditions of channels. Furthermore, our results provide an explanation for why calcium oscillations on both sides of the nuclear envelope may be beneficial for sustained perinuclear signaling.Electronic supplementary materialThe online version of this article (doi:10.1186/s12918-016-0289-9) contains supplementary material, which is available to authorized users.

Nucleobindin 1 (NUCB1) is a Golgi-resident marker of neurons

Nucleobindin 1 (NUCB1; also known as CALNUC or NUC) is a putative DNA- and calcium-binding protein and exhibits significant structural homology with the protein nucleobindin 2 (NUCB2; also known as nesfatin). While NUCB2 has been mapped in detail in the brain and implicated in the hypothalamic control of energy metabolism, no study has to date addressed the presence of NUCB1 in the central nervous system. Here we have explored the expression and distribution of NUCB1 in the rat brain and spinal cord, using RT-PCR, immunofluorescence and in situ hybridization.NUCB1 mRNA and protein was found to be present in all brain regions, extending to the spinal cord and dorsal root ganglia. Double-staining for NUCB1 and NeuN, glial fibrillary acidic protein and myelin basic protein revealed that NUCB1 is exclusively found in neurons, and not in glial or ependymal cells. Notably, NUCB1-immunoreactivity was observed in all neurons examined, making no distinction between previously identified glutamatergic and GABAergic populations, including those that are known not to stain for NeuN. This included the markedly more restricted population of NUCB2-expressing neurons in the brain. The protein was detected in cell somata and proximal dendrites, but not in axons or terminal structures. Further examination of the subcellular distribution of NUCB1 using organelle-specific markers revealed its consistent presence in the Golgi apparatus.These findings identify NUCB1 as a novel pan-neuronal marker. Along with the recent demonstration of broad expression of the protein in endocrine cells, the present results suggest that NUCB1 may play a role in spatiotemporal calcium handling in signaling cells.

Protein ligand-tethered synthetic calcium indicator for localization control and spatiotemporal calcium imaging in plant cells.

In plant biology, calcium ions are involved in a variety of intriguing biological phenomena as a secondary messenger. However, most conventional calcium indicators are not applicable for plant cells because of the difficulty with their localization control in plant cells. We here introduce a method to monitor spatiotemporal Ca(2+) dynamics in living plant cells based on linking the synthetic calcium indicator Calcium Green-1 to a natural product-based protein ligand. In a proof-of-concept study using cultured BY-2 cells overexpressing the target protein for the ligand, the ligand-tethered probe accumulated in the cytosol and nucleus, and enabled real-time monitoring of the cytosolic and nucleus Ca(2+) dynamics under the physiological condition. The present strategy using ligand-tethered fluorescent sensors may be successfully applied to reveal the spatiotemporal dynamics of calcium ions in living plant cells.

Finite Element Model to Study One Dimensional Calcium Dyanmics in Cardiac Myocytes

The multi physical process involving calcium ions regulate expansion and contraction of cardiac myocytes. This mechanism of expansion and contraction of cardiac myocytes is responsible for contraction and expansion of heart for pumping of blood into arteries and receiving blood into heart from vein. Thus calcium dynamics in cardiac myocytes is responsible for the activities of the myocytes cells and functioning of the heart. The specific spatiotemporal calcium ion dynamics is required to trigger, sustain and terminate activity of the cell. In this paper an attempt has been done to propose a model to study calcium dynamics in cardiac myocytes for a one-dimensional unsteady state case. The model incorporates the process like diffusion, reaction involving source and excess buffers. Appropriate boundary conditions and initial conditions have been framed. The finite element method has been employed to obtain the solution. The numerical results have been used to study the effect of buffers and source influx on calcium dynamics in cardiac myocytes.