Structure and Function of the Egg Cortex from Oogenesis through Fertilization

Sardet, Christian; Prodon, François; Dumollard, Rémi; Chang, Patrick; Chênevert, Janet

doi:10.1006/dbio.2001.0474

Cited by 95 publications

(53 citation statements)

References 252 publications

(294 reference statements)

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“…34). In addition to supporting layers of exocytotic vesicle populations (30), it also hosts the [Ca 2ϩ ] i cortical flash (4,5), a unique tubular endoplasmic reticulum morphology with an exclusive complement of luminal Ca 2ϩ -binding proteins (35,36), as well as a greater density of ryanodine receptors (37).…”

Section: Discussionmentioning

confidence: 99%

Fertilization and Nicotinic Acid Adenine Dinucleotide Phosphate Induce pH Changes in Acidic Ca2+ Stores in Sea Urchin Eggs

Morgan

Galione

2007

Journal of Biological Chemistry

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The second messenger nicotinic acid adenine dinucleotide phosphate (NAADP) releases Ca 2؉ from the acidic Ca 2؉ stores of many organisms, including those of the sea urchin egg. We investigated whether the pH within the lumen of these acidic organelles changes in response to stimuli. Fertilization activates the egg by Ca 2؉ release dependent upon NAADP, and accordingly, we report that fertilization also alters organellar pH in a spatio-temporally complex manner. Upon sperm fusion, vesicles deep in the egg center slowly acidify, whereas cortical vesicles undergo a rapid alkalinization. The cortical vesicle alkalinization is independent of exocytosis and cytosolic pH but coincides with the NAADP-dependent fertilization Ca 2؉ wave. Microinjection of NAADP mimicked the fertilization cortical response, suggesting that it occurred within NAADP-sensitive acidic Ca 2؉ stores. Our data show that NAADP and physiological stimuli alter the pH within intracellular organelles and suggest that NAADP signals through pH as well as Ca 2؉ .The sea urchin egg is an invaluable cell model for studying Ca 2ϩ signaling since the discovery of new second messengers and new Ca 2ϩ stores in this system has subsequently proven to have a major impact on mammalian biology (1). The mechanism of activation of the egg upon fertilization encompasses the rapid increases in the cytosolic pH and intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) important for fertilization envelope formation, DNA and protein synthesis, and embryological development (2). The pattern of [Ca 2ϩ ] i changes within the egg are highly organized spatio-temporally and reflect the precisely timed and placed recruitment of different families of Ca 2ϩ channels resident upon either the plasma membrane or intracellular organelles (2, 3). After the initial transient "cortical flash" caused by Ca 2ϩ influx across the plasma membrane (2-5), Ca 2ϩ release from intracellular stores is manifest as a Ca 2ϩ wave that propagates across the entire egg initiating from the point of sperm entry (2). These phasic elevations in [Ca 2ϩ ] i are driven by a complex interplay between the second messengers inositol 1,4,5-trisphosphate, cyclic adenosine diphosphoribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) 2 (1). Importantly, the relative contribution of each messenger to each phase of the Ca 2ϩ signal is different, e.g. NAADP is the only messenger implicated in the cortical flash (4, 5), whereas cyclic adenosine diphosphoribose probably plays a later role in prolonging the main Ca 2ϩ spike (6).NAADP not only evokes a cortical flash but, as first revealed in sea urchin egg, also releases Ca 2ϩ from acidic Ca 2ϩ stores that are lysosome-like organelles (possibly yolk platelets in eggs), whereas inositol 1,4,5-trisphosphate and cyclic adenosine diphosphoribose release Ca 2ϩ from the neutral endoplasmic reticulum (1, 7). Recently in sea urchin egg homogenate, we revealed that the luminal pH (pH L ) of these acidic stores is dynamic and increases upon NAADP-induced Ca 2ϩ release, whic...

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Section: Discussionmentioning

confidence: 99%

Fertilization and Nicotinic Acid Adenine Dinucleotide Phosphate Induce pH Changes in Acidic Ca2+ Stores in Sea Urchin Eggs

Morgan

Galione

2007

Journal of Biological Chemistry

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“…As a result, symmetric division took place. During mitosis, spindle positioning involves a cortical-microtubule capture mechanism and several proteins are involved in the interaction between microtubules and the cortex [26,27]. In Saccharomyces cerevisiae, microtubule cortical attachment includes mediation by actin, Kar9p, Bud6p and Bni1p [28,29].…”

Section: Discussionmentioning

confidence: 99%

Effects of MEK inhibitor U0126 on meiotic progression in mouse oocytes: microtuble organization, asymmetric division and metaphase II arrest

et al. 2003

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In this study we used U0126, a potent and specific inhibitor of MEK, to study the roles of MEK/ERK/p90 rsk signaling pathway in the meiotic cell cycle of mouse oocytes. The phosphorylation of MAP kinase and p90 rsk in the oocytes treated with 1.5 M U0126 was the same as that in oocytes cultured in drug-free medium. With 1.5 M U0126 treatment, the spindles appeared normal as they formed in oocytes, but failed to maintain its structure. Instead, the spindle lost one pole or elongated extraordinarily. After further culture, some oocytes extruded gigantic polar bodies (>30 m) that later divided into two small ones. Some oocytes underwent symmetric division and produced two equal-size daughter cells in which normal spindles formed. In oocytes with different division patterns, MAP kinase was normally phosphorylated. When the concentration of U0126 was increased to 15 M, the phosphorylation of both MAPK and p90 rsk were inhibited, while symmetric division was decreased. When incubating in medium containing 15 M U0126 for 14 h, oocytes were activated, but part of them failed to emit polar bodies. MII oocytes were also activated by 15 M U0126, at the same time the dephosphorylation of MAP kinase and p90 rsk was observed. Our results indicate that 1) MEK plays important but not indispensable roles in microtubule organization; 2) MEK keeps normal meiotic spindle morphology, targets peripheral spindle positioning and regulates asymmetric division by activating some unknown substrates other than MAP kinase /p90 rsk ; and 3) activation of MEK/ERK/p90 rsk cascade maintains MII arrest in mouse oocytes.

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“…CG exocytosis is another event of egg activation that depends on Ca 2þ release (Kline and Kline 1992a). CG release underlies, at least in part, the cortical remodeling that occurs after fertilization (Sardet et al 2002), and modifies the components of zona pellucida to prevent polyspermy, thereby ensuring the formation of a diploid zygote. Although it was believed that the effects of Ca 2þ on CGs were transduced by activation of protein kinase C (PKC), as PKC agonists promoted CG release and other activation events, later studies using PKC inhibitors failed to prevent fertilization-associated CG release (Ducibella and LeFevre 1997).…”

Section: Egg Activationmentioning

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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Structure and Function of the Egg Cortex from Oogenesis through Fertilization

Cited by 95 publications

References 252 publications

Fertilization and Nicotinic Acid Adenine Dinucleotide Phosphate Induce pH Changes in Acidic Ca2+ Stores in Sea Urchin Eggs

Fertilization and Nicotinic Acid Adenine Dinucleotide Phosphate Induce pH Changes in Acidic Ca2+ Stores in Sea Urchin Eggs

Effects of MEK inhibitor U0126 on meiotic progression in mouse oocytes: microtuble organization, asymmetric division and metaphase II arrest

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

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