Effect on Sperm-Induced Activation Current and Increase of Cytosolic Ca2+by Agents That Modify the Mobilization of [Ca2+]i

Mohri, Tatsuma; Ivonnet, Pedro; Chambers, Edward L.

doi:10.1006/dbio.1995.0011

Cited by 66 publications

(72 citation statements)

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“…3a) and the cortical exocytosis reaction (not shown) previously documented by others (22)(23)(24). The height of the peak produced by Ins-P 3 reached a maximum of 1.2 arbitrary units, the Ca 2ϩ increase lasting about 7 min.…”

Section: Resultssupporting

confidence: 68%

Nicotinic Acid Adenine Dinucleotide Phosphate-induced Ca2+ Release

Santella¹,

Kyozuka²,

Genazzani³

et al. 2000

Journal of Biological Chemistry

101

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Section: Resultssupporting

confidence: 68%

Nicotinic Acid Adenine Dinucleotide Phosphate-induced Ca2+ Release

Santella¹,

Kyozuka²,

Genazzani³

et al. 2000

Journal of Biological Chemistry

101

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“…Studies have shown that microinjection of the InsP 3 receptor antagonist heparin in conjunction with antagonists of the ryanodine receptor, such as ruthenium red and the cADPR inhibitor 8-amino-cADPR, block the Ca 2ϩ transient at fertilization (10,11). Injection with heparin alone, unless used at relatively high concentrations (12), does not abolish the fertilization Ca 2ϩ transient (10,11,13). cADPR and ryanodine receptor antagonists block the transient only in the presence of InsP 3 antagonists (10,11), if at all (14).…”

mentioning

confidence: 99%

“…InsP 3 is produced by members of the phosphatidylinositol phospholipase C (PLC) enzyme family and has been shown to be generated at fertilization (15)(16)(17)(18). Chemical inhibitors of PLC, pentosan polysulfate and U73122, can abolish fertilization Ca 2ϩ transients in sea urchin eggs (12,17). Molecular inhibition studies, using dominant negative PLC␥SH2 domain constructs, show that sperm-activated Ca 2ϩ release and egg activation are markedly delayed, then blocked, when activation of this enzyme is inhibited (19 -21).…”

mentioning

confidence: 99%

The NO Pathway Acts Late during the Fertilization Response in Sea Urchin Eggs

Leckie

Empson

Becchetti

et al. 2003

Journal of Biological Chemistry

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Both the inositol 1,4,5-trisphosphate (InsP 3 ) and ryanodine receptor pathways contribute to the Ca 2؉ transient at fertilization in sea urchin eggs. To date, the precise contribution of each pathway has been difficult to ascertain. Evidence has accumulated to suggest that the InsP 3 receptor pathway has a primary role in causing Ca 2؉ release and egg activation. However, this was recently called into question by a report implicating NO as the primary egg activator. In the present study we pursue the hypothesis that NO is a primary egg activator in sea urchin eggs and build on previous findings that an NO/cGMP/cyclic ADP-ribose (cADPR) pathway is active at fertilization in sea urchin eggs to define its role. Using a fluorescence indicator of NO levels, we have measured both NO and Ca 2؉ at fertilization and establish that NO levels rise after, not before, the Ca 2؉ wave is initiated and that this rise is Ca 2؉ -dependent. By inhibiting the increase in NO at fertilization, we find not that the Ca 2؉ transient is abolished but that the duration of the transient is significantly reduced. The latency and rise time of the transient are unaffected. This effect is mirrored by the inhibition of cGMP and cADPR signaling in sea urchin eggs at fertilization. We establish that cADPR is generated at fertilization, at a time comparable to the time of the rise in NO levels. We conclude that NO is unlikely to be a primary egg activator but, rather, acts after the initiation of the Ca 2؉ wave to regulate the duration of the fertilization Ca 2؉ transient.

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“…The time of increase in ΔΨ m was also close to the value already mentioned using simultaneous measurements of ΔΨ m and [Ca 2+ ] i . The rise time of ΔNO, 53.5 s, has been previously reported around a peak of [Ca 2+ ] i by the method of simultaneous measurement of ΔNO and the activation current (AC) in a voltage-clamped egg because a peak of AC that corresponds to a peak of [Ca 2+ ] i (Mohri et al 1995 ;Mohri et al 2008 ).…”

Section: Timing Of δψ M and δNomentioning

confidence: 81%

Mitochondrial Activation and Nitric Oxide (NO) Release at Fertilization in Echinoderm Eggs

Mohri

Kyozuka

2014

Sexual Reproduction in Animals and Plants

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In the cell, mitochondria are important organelles to supply energy for essential cell activities. It is unclear when and how mitochondrial activity increases on fertilization. We refer to mitochondrial activation here as mitochondrial innermembrane hyperpolarization. We measured fl uorescence changes in mitochondrial inner-membrane potential (ΔΨ m ) during fertilization in eggs of the echinoderm Hemicentrotus pulcherrimus and the sand dollar Clypeaster japonicus using a mitochondrial dye, MitoTracker Red CMXR (MTR). Increase in fl uorescence was detected after insemination in most eggs, which indicates hyperpolarization in ΔΨ m . To obtain the relationship between changes in intracellular Ca 2+ ([Ca 2+ IntroductionFertilization is thought to be one of the most remarkable phenomena, in which a large amount of energy is required for a zygote to increase diverse cellular activities leading to structural and qualitative changes for development from a dormant unfertilized state. At fertilization, mitochondria could be signifi cant in increasing various cellular activities, including supplying the energy. Generally, mitochondria have been recognized as multifunctional organelles playing crucial roles in cellular control. Their roles are to provide the main cellular energy in the form of adenosine triphosphate (ATP), to generate and regulate reactive oxygen species, to buffer cytosolic Ca 2+ , and to regulate apoptosis through a mitochondrial permeability transition pore (Wallace et al. 2010 ). Therefore, it is assumed that mitochondrial activity should increase accompanying the sequential phenomena, called "egg activation," that comprise changes in intracellular concentration of Ca 2+ ([Ca 2+ ] i ), pH, nitric oxide (NO) release (ΔNO), other second-messenger signals, and cytoplasmic changes, leading to activation of many important enzymes and factors for development. In sea urchins, early studies on respiration demonstrated that a burst of respiration started immediately after fertilization and reached the peak level within 3 min (Foerder et al. 1978 ;Fujiwara and Yasumasu 1997 ;Warburg 1908 ). One third of the respiration at fertilization should be responsible for mitochondrial respiration. However, when and how the mitochondria really activate remains unclear. According to the chemiosmotic theory, measuring mitochondrial inner-membrane potential (ΔΨ m ) has been used as an index of mitochondrial activity because ΔΨ m is utilized to provide energy for ATP production (Solani et al. 2007 ). Mitochondrial activation is believed to be by changes in hyperpolarization of ΔΨ m (Fujihara et al. 2007 ). On the other hand, ΔNO at fertilization has been reported in sea urchin eggs, although its main function is still obscure (Leckie et al. 2003 ;Mohri et al. 2008 ). We found in our previous study that mitochondrial activity has some relationship to ΔNO because mitochondrial inhibitors such as CN − and NaN 3 inhibited ΔNO, and an egg stratifi ed by centrifugation showed colocalization by double-staining with the mito...

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Effect on Sperm-Induced Activation Current and Increase of Cytosolic Ca2+by Agents That Modify the Mobilization of [Ca2+]i

Cited by 66 publications

References 0 publications

Nicotinic Acid Adenine Dinucleotide Phosphate-induced Ca2+ Release

Nicotinic Acid Adenine Dinucleotide Phosphate-induced Ca2+ Release

The NO Pathway Acts Late during the Fertilization Response in Sea Urchin Eggs

Mitochondrial Activation and Nitric Oxide (NO) Release at Fertilization in Echinoderm Eggs

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