scholarly journals Multi-Cellular Functions of MG53 in Muscle Calcium Signaling and Regeneration

2020 ◽  
Vol 11 ◽  
Author(s):  
Dathe Z. Benissan-Messan ◽  
Hua Zhu ◽  
Weina Zhong ◽  
Tao Tan ◽  
Jianjie Ma ◽  
...  
Keyword(s):  
Calcium Signaling ◽  
Cellular Functions ◽  
Muscle Calcium

scholarly journals Functional Genomic Analysis of Fluconazole Susceptibility in the Pathogenic Yeast Candida glabrata: Roles of Calcium Signaling and Mitochondria

2004 ◽  
Vol 48 (5) ◽  
pp. 1600-1613 ◽  
Author(s):  
Rupinder Kaur ◽  
Irene Castaño ◽  
Brendan P. Cormack
Keyword(s):  
Calcium Signaling ◽  
Rna Polymerase Ii ◽  
Mitochondrial Function ◽  
Candida Glabrata ◽  
Genomic Analysis ◽  
Significant Loss ◽  
Cellular Functions ◽  
Pathogenic Yeast ◽  
Functional Genomic Analysis ◽  
Reversible Loss

ABSTRACT The pathogenic yeast Candida glabrata exhibits innate resistance to fluconazole, the most commonly used antifungal agent. By screening a library of 9,216 random insertion mutants, we identified a set of 27 genes which upon mutation, confer altered fluconazole susceptibility in C. glabrata. Homologues of three of these genes have been implicated in azole and/or drug resistance in Saccharomyces cerevisiae: two of these belong to the family of ABC transporters (PDR5 and PDR16), and one is involved in retrograde signaling from mitochondria to nucleus (RTG2). The remaining 24 genes are involved in diverse cellular functions, including ribosomal biogenesis and mitochondrial function, activation of RNA polymerase II transcription, nuclear ubiquitin ligase function, cell wall biosynthesis, and calcium homeostasis. We characterized two sets of mutants in more detail. Strains defective in a putative plasma membrane calcium channel (Cch1-Mid1) were modestly more susceptible to fluconazole but showed a significant loss of viability upon prolonged fluconazole exposure, suggesting that calcium signaling is required for survival of azole stress in C. glabrata. These mutants were defective in calcium uptake in response to fluconazole exposure. The combined results suggest that, in the absence of Ca2+ signaling, fluconazole has a fungicidal rather than a fungistatic effect on C. glabrata. The second set of mutants characterized in detail were defective in mitochondrial assembly and organization, and these exhibited very high levels of fluconazole resistance. Further analysis of these mutants indicated that in C. glabrata a mechanism exists for reversible loss of mitochondrial function that does not involve loss of mitochondrial genome and that C. glabrata can switch between states of mitochondrial competence and incompetence in response to fluconazole exposure.

Redox Regulation of Cardiac Muscle Calcium Signaling

2000 ◽  
Vol 2 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Martin Morad ◽  
Yuichiro J. Suzuki
Keyword(s):  
Calcium Signaling ◽  
Cardiac Muscle ◽  
Redox Regulation ◽  
Muscle Calcium

Calcium Signaling: Linking Environmental Signals to Cellular Functions

2000 ◽  
Vol 19 (4) ◽  
pp. 291-318 ◽  
Author(s):  
Sona Pandey ◽  
S. B. Tiwari ◽  
K. C. Upadhyaya ◽  
Sudhir K. Sopory
Keyword(s):  
Calcium Signaling ◽  
Cellular Functions ◽  
Environmental Signals

scholarly journals Postsynaptic CaV1.1-driven calcium signaling coordinates presynaptic differentiation at the developing neuromuscular junction

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Mehmet Mahsum Kaplan ◽  
Bernhard E. Flucher
Keyword(s):  
Neuromuscular Junction ◽  
Calcium Signaling ◽  
Motor Neurons ◽  
Motor Nerve ◽  
Neuromuscular Synapse ◽  
Presynaptic Differentiation ◽  
Motor Nerves ◽  
Muscle Calcium ◽  
Activity Dependent ◽  
Postsynaptic Target

AbstractProper formation of neuromuscular synapses requires the reciprocal communication between motor neurons and muscle cells. Several anterograde and retrograde signals involved in neuromuscular junction formation are known. However the postsynaptic mechanisms regulating presynaptic differentiation are still incompletely understood. Here we report that the skeletal muscle calcium channel (CaV1.1) is required for motor nerve differentiation and that the mechanism by which CaV1.1 controls presynaptic differentiation utilizes activity-dependent calcium signaling in muscle. In mice lacking CaV1.1 or CaV1.1-driven calcium signaling motor nerves are ectopically located and aberrantly defasciculated. Axons fail to recognize their postsynaptic target structures and synaptic vesicles and active zones fail to correctly accumulate at the nerve terminals opposite AChR clusters. These presynaptic defects are independent of aberrant AChR patterning and more sensitive to deficient calcium signals. Thus, our results identify CaV1.1-driven calcium signaling in muscle as a major regulator coordinating multiple aspects of presynaptic differentiation at the neuromuscular synapse.

scholarly journals The non-excitable smooth muscle: Calcium signaling and phenotypic switching during vascular disease

2008 ◽  
Vol 456 (5) ◽  
pp. 769-785 ◽  
Author(s):  
Suzanne J. House ◽  
Marie Potier ◽  
Jonathan Bisaillon ◽  
Harold A. Singer ◽  
Mohamed Trebak
Keyword(s):  
Smooth Muscle ◽  
Calcium Signaling ◽  
Vascular Disease ◽  
Phenotypic Switching ◽  
Muscle Calcium

scholarly journals Calcium signaling mediates mechanotransduction at the multicellular stage of Dictyostelium discoideum

2021 ◽  
Author(s):  
Hidenori Hashimura ◽  
Yusuke V. Morimoto ◽  
Yusei Hirayama ◽  
Masahiro Ueda
Keyword(s):  
Calcium Signaling ◽  
Dictyostelium Discoideum ◽  
Molecular Mechanisms ◽  
Calcium Release ◽  
Calcium Influx ◽  
Cytosolic Calcium ◽  
Calcium Signal ◽  
Mechanical Stimuli ◽  
Ip3 Receptor ◽  
Cellular Functions

Calcium acts as a second messenger and regulates cellular functions, including cell motility. In Dictyostelium discoideum, the cytosolic calcium level oscillates synchronously, and calcium signal waves propagate in the cell population during the early stages of development, including aggregation. At the unicellular phase, the calcium response through Piezo channels also functions in mechanosensing. However, calcium signaling dynamics during multicellular morphogenesis is still unclear. Here, live-imaging of cytosolic calcium levels revealed that calcium wave propagation, depending on cAMP relay, temporarily disappeared at the onset of multicellular body formation. Alternatively, the occasional burst of calcium signals and their propagation were observed in both anterior and posterior regions of migrating multicellular bodies. Calcium signaling in multicellular bodies occurred in response to mechanical stimulation. Both pathways, calcium release from the endoplasmic reticulum via IP3 receptor and calcium influx from outside the cell, were involved in calcium waves induced by mechanical stimuli. These show that calcium signaling works on mechanosensing in both the unicellular and multicellular phases of Dictyostelium using different molecular mechanisms during development.

scholarly journals Mitochondria, calcium homeostasis and calcium signaling

2016 ◽  
Vol 62 (3) ◽  
pp. 311-317 ◽  
Author(s):  
I.B. Zavodnik
Keyword(s):  
Calcium Signaling ◽  
Molecular Targets ◽  
Permeability Transition ◽  
Good Evidence ◽  
Cellular Functions ◽  
Pathological Conditions ◽  
Intracellular Signal ◽  
Permeability Transition Pores ◽  
And Control ◽  
Functional Mechanisms

Са2+ is a very important and versatile intracellular signal which controls numerous biochemical and physiological (pathophysiological) processes in the cell. Good evidence exists that mitochondria are sensors, decoders and regulators of calcium signaling. Precise regulation of calcium signaling in the cell involves numerous molecular targets, which induce and decode changes of Са2+ concentrations in the cell (pumps, channels, Са2+-binding proteins, Са2+-dependent enzymes, localized in the cytoplasm and organelles). Mitochondrial Са2+ uniporter accumulates excess of Са2+ in mitochondria, while Na+/Са2+- and H+/Са2+-antiporters extrude Са2+ in the cytoplasm. Mitochondrial Са2+ overloading results in formation of mitochondria permeability transition pores which play an important role in cell death under many pathological conditions. Mitochondria regulate Са2+ homeostasis and control important cellular functions such as metabolism, proliferation, survival. Identification of cellular and mitochondrial Ca2+ transporters and understanding their functional mechanisms open up new prospects for their using as therapeutic targets

Surface Structure of Nucleated Animal Cells: Carbon Replicas

1967 ◽  
Vol 25 ◽  
pp. 120-121
Author(s):  
Robert M. Glaeser ◽  
Thea B. Scott
Keyword(s):  
Cell Surface ◽  
Surface Structure ◽  
Particle Diameter ◽  
Cellular Functions ◽  
Animal Cells ◽  
Replica Technique ◽  
Carbon Replica ◽  
Characteristic Particle ◽  
Cell Surface Structure ◽  
Carbon Replicas

The carbon-replica technique can be used to obtain information about cell-surface structure that cannot ordinarily be obtained by thin-section techniques. Mammalian erythrocytes have been studied by the replica technique and they appear to be characterized by a pebbly or “plaqued“ surface texture. The characteristic “particle” diameter is about 200 Å to 400 Å. We have now extended our observations on cell-surface structure to chicken and frog erythrocytes, which possess a broad range of cellular functions, and to normal rat lymphocytes and mouse ascites tumor cells, which are capable of cell division. In these experiments fresh cells were washed in Eagle's Minimum Essential Medium Salt Solution (for suspension cultures) and one volume of a 10% cell suspension was added to one volume of 2% OsO4 or 5% gluteraldehyde in 0.067 M phosphate buffer, pH 7.3. Carbon replicas were obtained by a technique similar to that employed by Glaeser et al. Figure 1 shows an electron micrograph of a carbon replica made from a chicken erythrocyte, and Figure 2 shows an enlarged portion of the same cell.

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