Changes of free calcium levels with stages of the cell division cycle

Poenie, Martin; Alderton, Janet M.; Tsien, Roger Y.; Steinhardt, Richard A.

doi:10.1038/315147a0

Cited by 583 publications

(261 citation statements)

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“…Similar studies aimed at identifying Ca 2+ transients during the mitotic cell cycle of animal cells became possible with the development of membrane permeant Ca 2+ -sensitive fluorescent probes such as Fura-2 [47;48]. Ca 2+ transients associated with nuclear envelope breakdown, metaphase to anaphase transition and cytokinesis were observed [47][48][49]. Initial descriptive studies were followed by mechanistic experiments aimed at defining a causal relationship between the observed Ca 2+ transients during mitosis and subsequent cellular events.…”

Section: Ca 2+ Signals During Various Stages Of the Cell Cyclementioning

confidence: 99%

Ca2+ signaling, genes and the cell cycle

Machaca

2011

Cell Calcium

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Changes in the concentration and spatial distribution of Ca 2+ ions in the cytoplasm constitute a ubiquitous intracellular signaling module in cellular physiology. With the advent of Ca 2+ dyes that allow direct visualization of Ca 2+ transients, combined with powerful experimental tools such as electrophysiological recordings, intracellular Ca 2+ transients have been implicated in practically every aspect of cellular physiology, including cellular proliferation. Ca 2+ signals are associated with different phases of the cell cycle and interfering with Ca 2+ signaling or downstream pathways often disrupts progression of the cell cycle. Although there exists a dependence between Ca 2+ signals and the cell cycle the mechanisms involved are not well defined and given the cross-talk between Ca 2+ and other signaling modules, it is difficult to assess the exact role of Ca 2+ signals in cell cycle progression. Two exceptions however, include fertilization and T-cell activation, where well-defined roles for Ca 2+ signals in mediating progression through specific stages of the cell cycle have been clearly established. In the case of T-cell activation Ca 2+ regulates entry into the cell cycle through the induction of gene transcription.

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Section: Ca 2+ Signals During Various Stages Of the Cell Cyclementioning

confidence: 99%

Ca2+ signaling, genes and the cell cycle

Machaca

2011

Cell Calcium

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“…In addition to the rise in [Ca 2+ ]i during fertilization, multiple transient changes in [Ca 2+ ]i occur during the first cell cycle (Poenie et al 1986). These changes in [Ca 2+ ]i may regulate later developmental events, such as nuclear envelope breakdown (Steinhardt & Alderton 1988) and the onset of anaphase (Groigno & Whitaker 1998).…”

Section: Discussionmentioning

confidence: 99%

Protein tyrosine kinase‐dependent release of intracellular calcium in the sea urchin egg

1999

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The aminoguanide, methylglyoxal bis(guanylhydrazone) (MGBG), was shown to stimulate phosphorylation of RR-SRC, a synthetic protein tyrosine kinase (PTK) substrate, and different levels of tyrosyl phosphorylation of endogenous proteins in a sea urchin egg membrane-cortex preparation. Stimulating protein tyrosine kinase activity in the sea urchin egg stimulated intracellular Ca 2+ release, because microinjection of 1-5 mM of MGBG into unfertilized eggs triggered a transient rise in intracellular Ca 2+ activity ([Ca 2+ ]i) after a brief latent period. Pretreating eggs with PTK-specific inhibitors, genistein or tyrphostin B42, significantly inhibited the MGBG-induced rise in [Ca 2+ ]i. Methylglyoxal bis(guanylhydrazone) stimulation of PTK activities in the unfertilized sea urchin egg appeared to trigger Ca 2+ release through phospholipase C (PLC)-dependent inositol 1,4,5-trisphosphate (InsP3) production. The MGBG-induced Ca 2+ response could be suppressed in eggs preloaded with the InsP3 receptor antagonist, heparin, and was reduced in eggs pretreated with U73122, a PLC inhibitor. However, the response was unchanged in eggs treated with nicotinamide, an inhibitor of ADP-ribosyl cyclase, or nifedipine, an inhibitor of nicotinic acid adenine dinucleotide phosphate activity. These results suggest that MGBG may be useful as a chemical agonist of PTK in sea urchin eggs and allow direct testing of the PTK requirement for the transient rise in [Ca 2+ ]i in sea urchin eggs during fertilization. Although genistein was observed to significantly delay the onset, the sperm-induced Ca 2+ response in PTK inhibitor-loaded eggs otherwise appeared normal. Therefore, it was concluded that sea urchin eggs contain a PTK-dependent pathway that can mediate intracellular Ca 2+ release, but PTK activity does not appear to be required for the fertilization response.

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“…Thus, during the maturation process, the sensitivity of the actin cytoskeleton to Lat-A appears to be dependent on rearrangements of actin modulated by MPF. DISCUSSION A calcium increase in the perinuclear area where a variety of Ca 2ϩ stores are present (30) is required to trigger entry into the mitosis in early sea urchin embryos (31,32). Activation of calmodulin (CaM) occurs near the nuclear envelope just before mitosis entry (33).…”

Section: Modulation Of the Actin Cytoskeleton By Mpf Is Responsible Fmentioning

confidence: 99%

The M-phase-promoting Factor Modulates the Sensitivity of the Ca2+ Stores to Inositol 1,4,5-Trisphosphate via the Actin Cytoskeleton

Lim

Ercolano

Kyozuka³

et al. 2003

Journal of Biological Chemistry

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The resumption of the meiotic cycle (maturation) induced by 1-methyladenine in prophase-arrested starfish oocytes is indicated by the breakdown of the germinal vesicle and is characterized by the increased sensitivity of the Ca 2؉ stores to inositol 1,4,5-trisphosphate (InsP 3 ) to InsP 3 starting at the animal hemisphere (where the germinal vesicle was originally located) and propagating along the animal/vegetal axis of the oocyte. This initiates Ca 2؉ signals around the germinal vesicle before nuclear envelope breakdown. Previous studies have suggested that the final activation of the maturation-promoting factor (MPF), a cyclin-dependent kinase, which is the major element controlling the entry of eukaryotic cells into the M phase, occurs in the nucleus. MPF is then exported to the cytoplasm where its activity is autocatalytically amplified following a similar animal/vegetal spatial pattern. We have investigated whether activated MPF was involved in the increased sensitivity of the Ca 2؉ response to InsP 3 . We have found that the development of increased sensitivity of the Ca 2؉ stores to InsP 3 receptors together with the Ca 2؉ signals in the perinuclear region was blocked in oocytes treated with the specific MPF inhibitor roscovitine. That the nuclear MPF activation is indeed required for changes of the InsP 3 receptors sensitivity was shown by enucleating or by dissecting oocytes into vegetal and animal hemispheres prior to the addition of 1-MA. MPF activity 50 min after 1-methyladenine addition was much lower in the enucleated oocytes and in the vegetal hemisphere, which did not contain the germinal vesicle, as compared with the animal hemisphere, which did contain it. The Ca 2؉ increase induced by InsP 3 under these experimental conditions correlated with the changes in actin cytoskeleton induced by MPF.

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Changes of free calcium levels with stages of the cell division cycle

Cited by 583 publications

References 24 publications

Ca2+ signaling, genes and the cell cycle

Ca2+ signaling, genes and the cell cycle

Protein tyrosine kinase‐dependent release of intracellular calcium in the sea urchin egg

The M-phase-promoting Factor Modulates the Sensitivity of the Ca2+ Stores to Inositol 1,4,5-Trisphosphate via the Actin Cytoskeleton

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