Ionomycin, Thapsigargin, Ryanodine, and Sperm Induced Ca2+ Release Increase during Meiotic Maturation of Mouse Oocytes

Jones, Kevin; Carroll, John; Whittingham, D. G.

doi:10.1074/jbc.270.12.6671

Cited by 176 publications

(135 citation statements)

References 48 publications

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“…An increase in the sensitivity of IP 3 -dependent Ca 2þ release during oocyte maturation is a hallmark of Ca 2þ signaling differentiation in many species, including starfish (Chiba et al, 1990), hamster (Fujiwara et al, 1993), mouse (Jones et al, 1994;Mehlmann and Kline, 1994), and Xenopus (Terasaki et al, 2001;Machaca, 2004). However, the mechanisms underlying this enhanced Ca 2þ release are vaguely defined in the literature.…”

Section: Physiological Roles Of Ca 2r At Fertilizationmentioning

confidence: 94%

“…It is clear that Ca 2þ release through the IP 3 R is essential for egg activation at fertilization (Miyazaki et al, 1992;Kline and Kline, 1994). In contrast, the role of the RyR is contentious and seems to be more subtle in terms of regulating Ca 2þ -induced Ca 2þ release during the Ca 2þ oscillations that follow the initial Ca 2þ spike (Miyazaki et al, 1992Swann, 1992;Jones et al, 1994;Kline and Kline, 1994). In Xenopus, the situation is less complicated with only a single Ca 2þ release pathway detected functionally and biochemically, the type 1 IP 3 R (Parys et al, 1992;Parys and Bezprozvanny, 1995).…”

Section: Ca 2r Signalingmentioning

confidence: 99%

“…There is also a tendency for increased Ca 2þ store content during maturation, but its contribution to the enhanced Ca 2þ release in eggs appear to be small (Jones et al, 1994;Mehlmann and Kline, 1994;Jellerette et al, 2004;El Jouni et al, 2005).…”

Section: Physiological Roles Of Ca 2r At Fertilizationmentioning

confidence: 99%

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Ca²⁺ signaling differentiation during oocyte maturation

Machaca

2007

Journal Cellular Physiology

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Oocyte maturation is an essential cellular differentiation pathway that prepares the egg for activation at fertilization leading to the initiation of embryogenesis. An integral attribute of oocyte maturation is the remodeling of Ca 2þ signaling pathways endowing the egg with the capacity to produce a specialized Ca 2þ transient at fertilization that is necessary and sufficient for egg activation. Consequently, mechanistic elucidation of Ca 2þ signaling differentiation during oocyte maturation is fundamental to our understanding of egg activation, and offers a glimpse into Ca 2þ signaling regulation during the cell cycle.

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Section: Physiological Roles Of Ca 2r At Fertilizationmentioning

confidence: 94%

Section: Ca 2r Signalingmentioning

confidence: 99%

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Ca²⁺ signaling differentiation during oocyte maturation

Machaca

2007

Journal Cellular Physiology

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“…For example, in vitro fertilized mouse GV oocytes show fewer [Ca 2þ ] i oscillations and each [Ca 2þ ] i increase shows reduced duration and amplitude than those observed in fertilized MII eggs (Jones et al 1995a;Mehlmann et al 1996). The molecular events underlying these changes are not understood, although changes in IP 3 R1 sensitivity, i.e., the receptor's ability to conduct Ca 2þ in response to IP 3 , are thought to be involved.…”

Section: Ip 3 R1 In Maturing Oocytesmentioning

confidence: 99%

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

Wakai¹,

Vanderheyden²,

Fissore³

2011

Cold Spring Harbor Perspectives in Biology

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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...

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“…Furthermore, the interphase pronuclear embryos derived from parthenogenetic activation exhibit Ca 2+ oscillation at fertilization. This strongly suggests that the ability to generate Ca 2+ oscillation in response to fertlization is not restricted to the metaphse II eggs as was reported before [5,16]. What determines the intracellular Ca 2+ excitability of oocytes in response to fertilization?…”

Section: Discussionmentioning

confidence: 51%

The fertilization-induced Ca2+ oscillation in mouse oocytes is cytoplasmic maturation dependent

Deng

Sun

1996

Cell Res

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Mature eggs (at metaphase II stage) produce a series of Ca 2+ oscillation at fertilization. To define whether the fertilization-induced Ca 2+ oscillation is restrict to the metaphase II eggs and cell cycle dependent, mouse oocytes at prophase I (arrested at germinal vesicle stage), metaphase I, metaphase II, as well as the pronuclear embryos at interphase of the first mitotic division derived from fertilization or parthenogenetic activation were inseminated after removal of zona pellucida. The results show that the fertilization-induced Ca 2+ oscillation is not specific to metaphase II eggs. This is supported by the fact that immature oocytes generated the Ca 2+ oscillations at fertilization regardless of their nuclear progression from prophase I to metaphase I (in vitro matured) stage. More interestingly, it was first found that pronuclear embryos at interphase derived from parthenogenetic activation showed Ca 2+ oscillations in response to fertilization while the zygotes at interphase did not after reinsemination or intracytoplasmic injection of sperm extracts which induce Ca 2+ oscillations in MII eggs. This suggests that the ability of oocytes to generate Ca 2+ oscillation in response to sperm penetration is not regulated in a cell cycle dependent manner but dependent on the cytoplasmic maturation.

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Ionomycin, Thapsigargin, Ryanodine, and Sperm Induced Ca2+ Release Increase during Meiotic Maturation of Mouse Oocytes

Cited by 176 publications

References 48 publications

Ca²⁺ signaling differentiation during oocyte maturation

Ca²⁺ signaling differentiation during oocyte maturation

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

The fertilization-induced Ca2+ oscillation in mouse oocytes is cytoplasmic maturation dependent

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Ionomycin, Thapsigargin, Ryanodine, and Sperm Induced Ca2+ Release Increase during Meiotic Maturation of Mouse Oocytes

Cited by 176 publications

References 48 publications

Ca2+ signaling differentiation during oocyte maturation

Ca2+ signaling differentiation during oocyte maturation

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

The fertilization-induced Ca2+ oscillation in mouse oocytes is cytoplasmic maturation dependent

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Ca²⁺ signaling differentiation during oocyte maturation

Ca²⁺ signaling differentiation during oocyte maturation