Temporal and spatial dynamics of the periodic increase in intracellular free calcium at fertilization of golden hamster eggs

Miyazaki, Shunichi; Hashimoto, Naohiro; Yoshimoto, Yasuaki; Kishimoto, Takeo; Igusa, Yukio; Hiramoto, Yukio

doi:10.1016/0012-1606(86)90093-x

Cited by 299 publications

(117 citation statements)

References 17 publications

Supporting

Mentioning

112

Contrasting

Order By: Relevance

“…1A); these phenomena, which make possible the transition from egg to embryo, are collectively known as "egg activation" (Schultz and Kopf 1995;Stricker 1999;Ducibella et al 2002). As stated earlier, an increase in [Ca 2þ ] i is the universal trigger of egg activation in all species studied to date (Stricker 1999), and in mammals this signal adopts a pattern of brief but periodical increases in [Ca 2þ ] i that last for several hours after sperm entry (Miyazaki et al 1986). The spatiotemporal pattern of these [Ca 2þ ] i responses is decoded by downstream effectors, underpinning the distinct cellular events.…”

Section: Egg Activationmentioning

confidence: 87%

“…1A); these phenomena, which make possible the transition from egg to embryo, are collectively known as "egg activation" (Schultz and Kopf 1995;Stricker 1999; Ducibella et al 2002). As stated earlier, an increase in [Ca 2þ ] i is the universal trigger of egg activation in all species studied to date (Stricker 1999), and in mammals this signal adopts a pattern of brief but periodical increases in [Ca 2þ ] i that last for several hours after sperm entry (Miyazaki et al 1986 Release from the MII arrest is an early and necessary event of egg activation, as it allows completion of meiosis, establishment of euploidy and progression into interphase with DNA synthesis. The MII block is imposed at the conclusion of maturation prior to ovulation by the action of the cytostatic factor (CSF) (Masui and Markert 1971 ubiquitination and degradation of cyclin B (CycB).…”

mentioning

confidence: 81%

See 1 more Smart Citation

Ca2+ Signaling During Mammalian Fertilization: Requirements, Players, and Adaptations

Wakai¹,

Vanderheyden²,

Fissore³

2011

Cold Spring Harbor Perspectives in Biology

View full text Add to dashboard Cite

Changes in the intracellular concentration of calcium ([Ca 2þ ] i ) represent a vital signaling mechanism enabling communication among cells and between cells and the environment. The initiation of embryo development depends on a [Ca 2þ ] i increase(s) in the egg, which is generally induced during fertilization. The [Ca 2þ ] i increase signals egg activation, which is the first stage in embryo development, and that consist of biochemical and structural changes that transform eggs into zygotes. The spatiotemporal patterns of [Ca 2þ ] i at fertilization show variability, most likely reflecting adaptations to fertilizing conditions and to the duration of embryonic cell cycles. In mammals, the focus of this review, the fertilization [Ca 2þ ] i signal displays unique properties in that it is initiated after gamete fusion by release of a sperm-derived factor and by periodic and extended [Ca 2þ ] i responses. Here, we will discuss the events of egg activation regulated by increases in [Ca 2þ ] i , the possible downstream targets that effect these egg activation events, and the property and identity of molecules both in sperm and eggs that underpin the initiation and persistence of the [Ca 2þ ] i responses in these species.A n increase in the intracellular concentration of calcium ([Ca 2þ ] i ) underlies the initiation, progression and/or completion of a wide variety of cellular processes, including fertilization, muscle contraction, secretion, cell division, and apoptosis (Berridge et al. 2000). To survive and proliferate, cells and organisms must communicate, and changes in [Ca 2þ ] i allow them to quickly respond to environmental, nutritional, or ligand challenges with responses that regulate cell fate and function. Cells devote significant amounts of their energy reserves to create and maintain ionic gradients between extracellular and intracellular milieus and also within the latter, thereby allowing brief alterations in these gradients to have profound signaling effects. In the case of Ca 2þ , myriad proteins have acquired the ability to bind Ca 2þ , which allows them to interpret and transform these elevations into cellular functions. This review will examine the cellular modifications induced by [Ca 2þ ] i changes during fertilization in mature mammalian oocytes, henceforth referred to as eggs.Oocytes during maturation ready themselves for fertilization and the initiation of embryogenesis. During this transition, oocytes undergo changes that include the resumption and progression of meiosis, the development of polyspermy-preventing mechanisms, the reorganization of the cytoskeleton with spindle formation and displacement to the cortex, and the translation, accumulation, and degradation of specific mRNAs and proteins involved in development (Horner and Wolfner 2008b (Stricker 1999;Miyazaki and Ito 2006). Elucidation of the signaling cascades and identification of the molecules/receptor(s) that initiate the Ca 2þ signal at fertilization has proven elusive, and this review will not dwell on th...

show abstract

Section: Egg Activationmentioning

confidence: 87%

“…1A); these phenomena, which make possible the transition from egg to embryo, are collectively known as "egg activation" (Schultz and Kopf 1995;Stricker 1999; Ducibella et al 2002). As stated earlier, an increase in [Ca 2þ ] i is the universal trigger of egg activation in all species studied to date (Stricker 1999), and in mammals this signal adopts a pattern of brief but periodical increases in [Ca 2þ ] i that last for several hours after sperm entry (Miyazaki et al 1986 Release from the MII arrest is an early and necessary event of egg activation, as it allows completion of meiosis, establishment of euploidy and progression into interphase with DNA synthesis. The MII block is imposed at the conclusion of maturation prior to ovulation by the action of the cytostatic factor (CSF) (Masui and Markert 1971 ubiquitination and degradation of cyclin B (CycB).…”

mentioning

confidence: 81%

Ca2+ Signaling During Mammalian Fertilization: Requirements, Players, and Adaptations

Wakai¹,

Vanderheyden²,

Fissore³

2011

Cold Spring Harbor Perspectives in Biology

View full text Add to dashboard Cite

show abstract

“…Their amplitudes usually lie in the range 3Ϫ30 µM. The highest Ca 2ϩ values are found in the fertilization wave through the medaka egg (30 µM) [61,62], the fertilization wave through ascidian eggs (7Ϫ10 µM) [63], and the fertilization wave through the hamster eggs (5Ϫ10 µm) [64]. At these Ca 2ϩ levels, the activity of PLC δ3 is high (Fig.…”

Section: Discussionmentioning

confidence: 98%

Localization of phospholipase C δ3 in the cell and regulation of its activity by phospholipids and calcium

Pawełczyk

Matecki

1998

European Journal of Biochemistry

View full text Add to dashboard Cite

The localization of phospholipase C δ3 (PLC δ3) in the cell and its regulatory properties has been investigated. Western blotting showed that human platelet PLC δ3 is located in the membrane and cytosolic fraction. The enzyme amount in the cytosolic fraction was significantly lower than that in the membrane fraction. In rat liver, PLC δ3 was present in both the membrane and cytosolic fraction and was absent in nuclei. Examination of the effects of phospholipids on PLC δ3 revealed that this enzyme is inhibited by phosphatidylethanolamine (PtdEtn) and phosphatidylcholine (PtdCho). Similar inhibition was observed in the presence of sphingomyelin and phosphatidylserine (PtdSer). This is in contrast to PLC δ1, which is activated by PtdCho and PtdEtn. In a detergent assay, PLC δ1 is activated by spermine and sphingosine, whereas PLC δ3 was inhibited by both these compounds at concentrations that maximally stimulated PLC δ1. A deletion mutant of PLC δ3, lacking the entire pleckstrin homology (PH) domain (residues 1Ϫ137), was fully active in the detergent assay, and it was inhibited by spermine, sphingosine and phospholipids to the same extent as the native enzyme. PLC δ3 activation required calcium ions. The relationship between the Ca 2ϩ concentration and enzymatic activity was almost identical for the deletion mutant and the native enzyme. However, in the liposome assay, PLC δ3 was less sensitive to Ca 2ϩ stimulation. This is in contrast to PLC δ1, which is equally sensitive to Ca 2ϩ stimulation in both the detergent and liposome assays. We conclude that Ca 2ϩ is necessary to induce specific conformational changes of PLC δ3, which leads to a productive orientation of the catalytic domain relative to the membrane. The regulatory properties of PLC δ3 described in this report suggest that PLC δ3 has a relatively low activity in cellular conditions that fully activate PLC δ1.Keywords : phospholipase C δ3; platelets; localization; phospholipids ; calcium.Phospholipase C (PLC) hydrolyzes phosphatidylinositol located in cellular membranes to generate diacylglycerol and inositol 1,4,5-triphosphate (InsP 3 ). Diacylglycerol activates protein kinase C and InsP 3 mobilizes Ca 2ϩ from intracellular stores [1,2]. Changes in Ca 2ϩ and diacylglycerol levels affect virtually every aspect of cellular regulation directly or indirectly. The control of PLC activity is thus one of the major starting points for cellular regulation.To date, three major types of phosphoinositide-specific phospholipase C species named β, γ and δ, have been characterized [3,4]. Each type of PLC is regulated differently. PLC γ appears to be regulated by tyrosine phosphorylation in response to growth factor receptor occupancy [5]. The phosphorylation of PLC γ does not affect the kinetic properties of the enzyme, but causes a redistribution of the enzyme from the cytosol to cell membrane [6,7]. Tyrosine phosphorylation of PLC γ promotes its association with actin components of the cytoskeleton [8,9]. PLC β isozymes are activated by the A and βγ subunits of the h...

show abstract

“…In fertilized sea urchin and Xenopus eggs, the calcium increase takes the form of a propagating wave that originates at the point of sperm attachment and traverses the egg at a velocity of 5 to 10 µm/sec [1]. Studies in the hamster [2], mouse [3], cow [4] and pig [5] demonstrate that mammalian oocytes display a similar increase of intracellular calcium at fertilization, but that the initial transient rise is followed by a series of smaller transient increases. The frequency of the calcium transient increases, or oscillations, varies among species, occurring at intervals of 1 to 10 min in hamster oocytes [4] and 15 to 51 min in cattle oocytes [2].…”

mentioning

confidence: 99%

Calcium Release at Fertilization: Artificially Mimicking the Oocyte's Response to Sperm.

Grupen¹,

Nottle²,

Nagashima

2002

Journal of Reproduction and Development

View full text Add to dashboard Cite

Abstract. The mechanism of sperm-induced calcium release has been the subject of many studies since the development in the late 1950s of in vitro culture systems that support mammalian fertilization. Despite efforts to elucidate the nature of the signal from the sperm that triggers both the early and late events of oocyte activation, the precise mechanism remains unresolved. Now, with the advent of somatic nuclear transfer technologies, the need to better understand this unique process has been recognised. Nuclear transfer embryos must be induced to commence development artificially because the activating signal from the sperm is absent. The primary activating stimulus is a large increase in the concentration of intracellular-free calcium and numerous physical and chemical treatments have been found to induce calcium changes that initiate the events of oocyte activation. Although live cloned offspring have been produced in a number of species, the overall efficiencies of the nuclear transfer procedures described thus far are unacceptably low and phenotypic anomalies are common. With the aim of improving these efficiencies, researchers are developing artificial activation treatments which induce oocyte responses that mimic those induced by fertilizing sperm. One strategy is to replicate the pattern of calcium change more closely. Another strategy is to couple an activating stimulus with treatments that inhibit maturation (or M-phase) promoting factor (MPF) activity, which regulates meiotic progression in oocytes. This paper reviews what is understood of calcium release at fertilization and describes the treatments that have been used to induce oocyte activation artificially in parthenogenetic and nuclear transfer studies. The relative effectiveness of the strategies employed to mimic the oocyte's response to sperm are discussed. Key words: Oocyte activation, Fertilization, Parthenogenesis, Nuclear transfer (J. Reprod. Dev. 48: 2002) o produce a viable embryo at fertilization, the s p e r m n o t o n l y p r o v i d e s t h e m a l e chromosomal complement, but also the stimulus that initiates development. The mechanism by which the activating signal is transmitted from the sperm to the oocyte is not fully clarified, but it is clear that this signal triggers a large increase in the concentration of intracellular-free calcium. In fertilized sea urchin and Xenopus eggs, the calcium increase takes the form of a propagating wave that originates at the point of sperm attachment and traverses the egg at a velocity of 5 to 10 µm/sec

show abstract

Temporal and spatial dynamics of the periodic increase in intracellular free calcium at fertilization of golden hamster eggs

Cited by 299 publications

References 17 publications

Ca2+ Signaling During Mammalian Fertilization: Requirements, Players, and Adaptations

Ca2+ Signaling During Mammalian Fertilization: Requirements, Players, and Adaptations

Localization of phospholipase C δ3 in the cell and regulation of its activity by phospholipids and calcium

Calcium Release at Fertilization: Artificially Mimicking the Oocyte's Response to Sperm.

Contact Info

Product

Resources

About