Cell-cycle calcium transients driven by cyclic changes in inositol trisphosphate levels

Ciapa, Brigitte; Pesando, D.; Wilding, Martin; Whitaker, Michael

doi:10.1038/368875a0

Cited by 170 publications

(145 citation statements)

References 28 publications

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“…The overall reduction of I CRAC and relative low abundance of MagNuM in mitotic cells indicates that Ca 2+ influx plays a minor role during mitosis. This is in agreement with the observation that changes in intracellular Ca 2+ levels during mitosis are predominantly due to InsP 3 -induced Ca 2+ release but not influx [13,19,57].…”

Section: Discussionsupporting

confidence: 81%

Cell cycle-dependent regulation of store-operated ICRAC and Mg2+-nucleotide-regulated MagNuM (TRPM7) currents

et al. 2007

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Calcium signaling is a central mechanism for numerous cellular functions and particularly relevant for immune cell proliferation. However, the role of calcium influx in mitotic cell cycle progression is largely unknown. We here report that proliferating rat mast cells RBL-2H3 tightly control their major store-operated calcium influx pathway, I CRAC , during cell cycle progression. While I CRAC is maintained at control levels during the first gap phase (G1), the current is significantly upregulated in preparation for and during chromatin duplication. However, mitosis strongly suppresses I CRAC . Non-proliferating cells deprived of growth hormones strongly down-regulate I CRAC while increasing cell volume. We further show that the other known calcium (and magnesium) influx pathway in mast cells, the TRPM7-like magnesium-nucleotide-regulated metal (MagNuM) current, is largely uncoupled from cell cycle regulation except in G1. Taken together, our results demonstrate that both store-operated calcium influx via I CRAC and MagNuM are regulated at crucial checkpoints during cell cycle progression.

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Section: Discussionsupporting

confidence: 81%

Cell cycle-dependent regulation of store-operated ICRAC and Mg2+-nucleotide-regulated MagNuM (TRPM7) currents

et al. 2007

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“…The significance of this machinery within the nucleus has long been a question. Both growth factors (12) and integrins (36) InsP3 (16,37), plus temporally related increases in Ca 2ϩ in the perinuclear region (26,38,39), have been associated with breakdown of the nuclear envelope and entry into mitosis. In addition, nuclear Ca 2ϩ activates transcription factors such as CREB (9,11), Elk-1 (10), and DREAM (40), but cytosolic Ca 2ϩ activates other transcription factors such as SRE (9), plus phosphatases such as calcineurin that are important for transcription (41).…”

Section: Discussionmentioning

confidence: 99%

Nucleoplasmic Calcium Is Required for Cell Proliferation

Rodrigues

Gomes

Leite

et al. 2007

Journal of Biological Chemistry

121

176

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Ca2؉ signals regulate cell proliferation, but the spatial and temporal specificity of these signals is unknown. Here we use selective buffers of nucleoplasmic or cytoplasmic Ca 2؉ to determine that cell proliferation depends upon Ca 2؉ signals within the nucleus rather than in the cytoplasm. Nuclear Ca 2؉ signals stimulate cell growth rather than inhibit apoptosis and specifically permit cells to advance through early prophase. Selective buffering of nuclear but not cytoplasmic Ca 2؉ signals also impairs growth of tumors in vivo. These findings reveal a major physiological and potential pathophysiological role for nucleoplasmic Ca 2؉ signals and suggest that this information can be used to design novel therapeutic strategies to regulate conditions of abnormal cell growth. Ca2ϩ is a ubiquitous second messenger that mediates a wide range of cellular responses such as contraction, fluid and electrolyte secretion, exocytosis, gene transcription, and apoptosis (1). This ability to simultaneously control multiple processes occurs by careful modulation of Ca 2ϩ signals, not only over time but in different subcellular regions as well (2). For example, polarized Ca 2ϩ waves direct apical secretion in epithelia (3), whereas presynaptic increases in Ca 2ϩ trigger neurotransmitter release (4) and mitochondrial increases in Ca 2ϩ regulate apoptosis (5, 6). Ca 2ϩ signals also can be regulated independently in the nucleoplasm relative to the cytoplasm (7,8), but the physiological significance of this aspect of spatial control is not entirely understood. Nucleoplasmic Ca 2ϩ signals have distinct effects on activation of transcription factors (9, 10) and kinases (11, 12), but it is not known whether nuclear Ca 2ϩ signals also regulate more global aspects of cell function. Because cell proliferation (13,14) and progression through the cell cycle (15, 16) are Ca 2ϩ -dependent, we investigated the relative roles of nuclear and cytoplasmic Ca 2ϩ on cell growth. EXPERIMENTAL PROCEDURESMaterials, Reagents, and Cell Lines-SKHep1, HepG2, and HEK-293 cell lines were obtained from the American Type Culture Collection (Manassas, VA) and were used for all experiments. The cells were grown at 37°C with 5% CO 2 :95% O 2 in Dulbecco's modified Eagle's medium supplemented with 1% penicillin-streptomycin and 10% heat-inactivated fetal bovine serum, all from Invitrogen. The cells were grown on glass coverslips overnight in the absence of serum before infection with each parvalbumin (PV) 2 construct. Generation of Parvalbumin Constructs and AdenoviralInfection-Constructs encoding red fluorescence protein (DsRed) from Clontech (Mountain View, CA) and targeted PV proteins (PV-NLS, PV-NES, and PV-NLS-CD) were PCR-amplified and subcloned into pShuttle-CMV (kindly provided by Bert Vogelstein, Johns Hopkins) by restriction digestion with XhoI and XbaI to generate pShuttle-CMV-PVNLS-DSR, pShuttle-CMV-PVNES-DSR, and pShuttle-CMV-PVNLS-CD-DSR. Recombinant adenoviruses were generated by transformation of pShuttle-CMV-PV-NLS-DSR into AdEasier-1 cells, a deri...

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“…The events of fertilization may be directly or indirectly due to phosphatidylinositol 4,5-bisphosphate (PIP2)' breakdown to inositol 1,4,5-trisphosphate (IP3) and sn-1,2-diacylglycerol (DAG; Turner et al, 1984;Whitaker and Irvine, 1984;Kamel et al, 1985;LePeuch et al, 1985;Ciapa et al, 1992, Stith et al, 1993Ciapa et al, 1994). A sperm-induced increase in IP3 and intracellular calcium ([Ca2+I1) are thought to be responsible for fertilization events such as membrane depolarization, cortical granule breakdown, intracellular pH increase, and the induction of other developmental events (for Xenopus, Busa et al, 1985a,b; Kline, 1988;Grandin and Charbonneau, 1992).…”

Section: Introductionmentioning

confidence: 99%

sn-1,2-diacylglycerol and choline increase after fertilization in Xenopus laevis.

Stith

Woronoff

Espinoza

et al. 1997

MBoC

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sn-1,2-Diacylglycerol (DAG) mass and translocation of protein kinase C a and ,B to a membrane fraction increased -7 min after insemination of Xenopus laevis eggs. The DAG mass increase of 48 pmol (from 62 to 110 pmol/cell) was greater than that for inositol 1,4,5-trisphosphate (1P3; an increase of -170 fmol or -280-fold smaller than the DAG increase), and DAG peaks -5 min after IP3. Choline mass (a measure of phosphatidylcholine-specific phospholipase D) also peaked before DAG and the choline increase (134 pmol/cell) was greater than that of DAG. There was no detectable change in phosphocholine mass (a measure of phosphatidylcholine-specific phospholipase C). During first cleavage, DAG decreased, PKC translocation was low, and choline increased and peaked (whereas published work shows an increase in IP3 mass). Artificial elevation of intracellular calcium ([Ca2+]

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Cell-cycle calcium transients driven by cyclic changes in inositol trisphosphate levels

Cited by 170 publications

References 28 publications

Cell cycle-dependent regulation of store-operated ICRAC and Mg2+-nucleotide-regulated MagNuM (TRPM7) currents

Cell cycle-dependent regulation of store-operated ICRAC and Mg2+-nucleotide-regulated MagNuM (TRPM7) currents

Nucleoplasmic Calcium Is Required for Cell Proliferation

sn-1,2-diacylglycerol and choline increase after fertilization in Xenopus laevis.

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