Cell cycle-dependent Ca2+ oscillations in mouse embryos are regulated by nuclear targeting of PLCζ

Larman, Mark G.; Saunders, Christopher P.; Carroll, John; Lai, F. Anthony; Swann, Karl

doi:10.1242/jcs.01109

Cited by 124 publications

(116 citation statements)

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“…Repetitive Ca 2+ oscillations occur immediately following fertilisation in mammalian oocytes, and are believed to be driven by InsP 3 production that is caused by the introduction of PtdIns-PLCζ into the oocyte from the fused sperm. The Ca 2+ oscillations cease around the time when the pronucleus is formed, owing to the sequestration of PtdIns-PLCζ in the nucleus (Larman et al, 2004). Unlike the other PtdIns-PLC isozymes described above, when PtdIns-PLCζ is in the nucleus, it does not evoke InsP 3 production and Ca 2+ signalling.…”

Section: Autonomous Generation Of Ca 2+ -Mobilising Messengers In Thementioning

confidence: 89%

An update on nuclear calcium signalling

Bootman

Fearnley

Smyrnias

et al. 2009

Journal of Cell Science

189

194

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Over the past 15 years or so, numerous studies have sought to characterise how nuclear calcium (Ca 2+ ) signals are generated and reversed, and to understand how events that occur in the nucleoplasm influence cellular Ca 2+ activity, and vice versa. In this Commentary, we describe mechanisms of nuclear Ca 2+ signalling and discuss what is known about the origin and physiological significance of nuclear Ca 2+ transients. In particular, we focus on the idea that the nucleus has an autonomous Ca 2+ signalling system that can generate its own Ca 2+ transients that modulate processes such as gene transcription. We also discuss the role of nuclear pores and the nuclear envelope in controlling ion flux into the nucleoplasm. Journal of Cell Science 2338(which would cause its nuclear export) and through a physical interaction that occludes a nuclear-export sequence (NES) in the NFAT protein.An example of a nuclear-localised transcription factor that is regulated by both nuclear and cytosolic Ca 2+ signals is cyclic AMP response element-binding protein (CREB). The signalling mechanisms that underlie CREB activation have been worked out particularly well in neurons, in which it has been established that depolarisation leads to the rapid phosphorylation of CREB on Ser133 by Ca 2+ -calmodulin-dependent kinase IV, which provides a necessary, but not sufficient, signal for CREB-mediated gene transcription (Dolmetsch et al., 2001). The triggering event is an increase in cytosolic Ca 2+ levels in the immediate vicinity of L-type Ca 2+ channels or N-methyl-D-aspartate receptors that are found in the synapse, at a site that is distal to the nucleus (Shaywitz and Greenberg, 1999). As CREB is only found in the nucleus, the phosphorylation of Ser133 is mediated by one of several Ca 2+ -sensitive signal transduction cascades that convey information from the remote synapses into the nucleus. In the nucleus, phosphorylated CREB binds additional proteins to form a transcriptionally active complex (Shaywitz and Greenberg, 1999). Although the synaptic Ca 2+ signal does not need to propagate to the nucleus to induce phosphorylation of Ser133 on CREB, an increase in the level of nuclear Ca 2+ is required for CREB-mediated gene transcription to occur. This is because additional Ca 2+ -dependent phosphorylation of CREB and its co-activators is required (Chawla et al., 1998;Kornhauser et al., 2002). Indeed, nuclear injection of an artificial Ca 2+ buffer prevents CREB-mediated gene transcription, but not transcription induced by the serum-response element, which is sensitive to cytosolic Ca 2+ buffering (Hardingham et al., 1997).Another well-known target of nuclear Ca 2+ signalling is the transcriptional regulator downstream regulatory element antagonist modulator (DREAM). It is well established that DREAM represses the expression of prodynorphin, an opiate-receptor precursor, and that mice that lack DREAM have a constitutive analgesic condition (Cheng et al., 2002). DREAM contains four Ca 2+ -binding EF hands (a widely expressed structural mo...

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Section: Autonomous Generation Of Ca 2+ -Mobilising Messengers In Thementioning

confidence: 89%

An update on nuclear calcium signalling

Bootman

Fearnley

Smyrnias

et al. 2009

Journal of Cell Science

189

194

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“…Larman et al addressed this question in a 2004 study [14]. They observed that Ca 2+ oscillation was obtained pluripotency, we must understand the two-calcium-pool model of Ca 2+ oscillation, because Ca 2+ oscillation is thought to be a necessary and sufficient condition in the creation of pluripotency.…”

Section: A Role For Cell's Water Property In Proton/calcium Signalingmentioning

confidence: 99%

“…What is the difference between the two (M vs. G1/G2)? A few hypotheses have been put forth [14,15], but in the next section we propose a new model based on the water state in the cell.…”

Section: Introductionmentioning

confidence: 99%

A Role for Proton Signaling in the Induction of Somatic Cells to Pluripotent Embryonic Stem Cells

Yoshioka¹

2014

J Phys Chem Biophys

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“…After a false start (Parrington et al 1996;Shevchenko et al 1998), the active component was identified as a novel phospholipase C, PLCz, that was present only in the testis and the sperm (Rice et al 2000;Saunders et al 2002). This entirely specific tissue distribution argues very strongly that PLCz is the activating agent in mammalian fertilization; there is other indirect evidence: PLCz is sequestered into the zygote nucleus as it reforms after fertilization just as the fertilization calcium transients are dying away; if sequestration is prevented, the transients persist (Kono et al 1995;Larman et al 2004;Saunders et al 2007). It has to be admitted though that the definitive proof by gene knockout is lacking.…”

Section: Initiation and Propagation Of The Fertilization Calcium Wavementioning

confidence: 99%

Calcium signalling in early embryos

Whitaker

2008

Phil. Trans. R. Soc. B

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The onset of development in most species studied is triggered by one of the largest and longest calcium transients known to us. It is the most studied and best understood aspect of the calcium signals that accompany and control development. Its properties and mechanisms demonstrate what embryos are capable of and thus how the less-understood calcium signals later in development may be generated. The downstream targets of the fertilization calcium signal have also been identified, providing some pointers to the probable targets of calcium signals further on in the process of development.In one species or another, the fertilization calcium signal involves all the known calcium-releasing second messengers and many of the known calcium-signalling mechanisms. These calcium signals also usually take the form of a propagating calcium wave or waves.Fertilization causes the cell cycle to resume, and therefore fertilization signals are cell-cycle signals. In some early embryonic cell cycles, calcium signals also control the progress through each cell cycle, controlling mitosis.Studies of these early embryonic calcium-signalling mechanisms provide a background to the calcium-signalling events discussed in the articles in this issue.

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Cell cycle-dependent Ca2+ oscillations in mouse embryos are regulated by nuclear targeting of PLCζ

Cited by 124 publications

References 41 publications

An update on nuclear calcium signalling

An update on nuclear calcium signalling

A Role for Proton Signaling in the Induction of Somatic Cells to Pluripotent Embryonic Stem Cells

Calcium signalling in early embryos

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