TRPV3 Channels Mediate Strontium-Induced Mouse-Egg Activation

Carvacho, Ingrid; Lee, Hoi Chang; Fissore, Rafael A.; Clapham, David E.

doi:10.1016/j.celrep.2013.11.007

Cited by 68 publications

(104 citation statements)

References 79 publications

(91 reference statements)

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“…We hypothesized that transient receptor potential (TRP) channels were likely candidates for this role because these cation conducting channels are expressed in all types of cells and can contribute to a wide array of cellular responses (reviewed in [33]). TRPV3 current has been demonstrated in mouse eggs, but this current was not detected in GV oocytes [34]; therefore, TRPV3 is unlikely to mediate spontaneous Ca 2+ influx in GV oocytes. Mice lacking all seven TRPC channels have been generated and shown to be viable and fertile [35].…”

Section: Resultsmentioning

confidence: 99%

“…We previously demonstrated that Ca V 3.2 contributes to Ca 2+ influx to support ER store accrual and robust Ca 2+ oscillations, but females lacking Ca V 3.2 are merely subfertile, indicating that this channel does not function alone either [27]. TRPV3 channels are present in mouse eggs and contribute to Sr 2+ -mediated parthenogenesis; however, Trpv3 −/− females are fertile and their eggs have normal Ca 2+ oscillations following fertilization, indicating that these channels do not have a required physiological function in eggs [34]. It will be interesting to begin investigating the effects of knocking out these channels in combination to overcome inherent limitations of studies using pharmacological inhibitors and ultimately determine the mechanisms of Ca 2+ influx that support egg activation.…”

Section: Discussionmentioning

confidence: 99%

“…Overexpression of SOCE components in oocytes and eggs enhances the magnitude of SOCE-like responses and impacts Ca 2+ oscillations and influx, indicating that SOCE components can function in eggs when expressed at supra-physiological levels [1, 15]. Furthermore, while some effects of 2-APB on oocyte and egg responses can be explained by modulation of TRPM7 or TRPV3 channels, it is possible that this inhibitor also impacts SOCE-like responses in other ways in these cells [1, 15, 34, 37]. Thus, it is apparent that the status of ER Ca 2+ stores influences Ca 2+ influx regulation in mouse oocytes and eggs, but this effect is not mediated by STIM-ORAI interaction.…”

Section: Discussionmentioning

confidence: 99%

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Store-operated Ca 2+ entry is not required for fertilization-induced Ca 2+ signaling in mouse eggs

et al. 2017

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Repetitive oscillations in cytoplasmic Ca2+ due to periodic Ca2+ release from the endoplasmic reticulum (ER) drive mammalian embryo development following fertilization. Influx of extracellular Ca2+ to support the refilling of ER stores is required for sustained Ca2+ oscillations, but the mechanisms underlying this Ca2+ influx are controversial. Although store-operated Ca2+ entry (SOCE) is an appealing candidate mechanism, several groups have arrived at contradictory conclusions regarding the importance of SOCE in oocytes and eggs. To definitively address this question, Ca2+ influx was assessed in oocytes and eggs lacking the major components of SOCE, the ER Ca2+ sensor STIM proteins, and the plasma membrane Ca2+ channel ORAI1. We generated oocyte-specific conditional knockout (cKO) mice for Stim1 and Stim2, and also generated Stim1/2 double cKO mice. Females lacking one or both STIM proteins were fertile and their ovulated eggs displayed normal patterns of Ca2+ oscillations following fertilization. In addition, no impairment was observed in ER Ca2+ stores or Ca2+ influx following store depletion. Similar studies were performed on eggs from mice globally lacking ORAI1; no abnormalities were observed. Furthermore, spontaneous Ca2+ influx was normal in oocytes from Stim1/2 cKO and ORAI1-null mice. Finally, we tested if TRPM7-like channels could support spontaneous Ca2+ influx, and found that it was largely prevented by NS8593, a TRPM7-specific inhibitor. Fertilization-induced Ca2+ oscillations were also impaired by NS8593. Combined, these data robustly show that SOCE is not required to support appropriate Ca2+ signaling in mouse oocytes and eggs, and that TRPM7-like channels may contribute to Ca2+ influx that was previously attributed to SOCE.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Store-operated Ca 2+ entry is not required for fertilization-induced Ca 2+ signaling in mouse eggs

et al. 2017

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“…The nonselective, Ca 2þ -permeant transient receptor potential (TRP) channels are intriguing candidates to be these mechanosensitive channels [69,84,86,88]. However, little is known about TRP channels in mammalian eggs; only TRPV3 is thus far characterized in mouse eggs, and its role in normal egg activation is unclear (but TRPV3 does appears to mediate Sr 2þ influx in SrCl 2 -induced artificial egg activation) [89]. It is very likely that multiple channels could mediate Ca 2þ influx into eggs.…”

Section: Discussionmentioning

confidence: 98%

MAPK3/1 (ERK1/2) and Myosin Light Chain Kinase in Mammalian Eggs Affect Myosin-II Function and Regulate the Metaphase II State in a Calcium- and Zinc-Dependent Manner1

McGinnis

Lee

Robinson

et al. 2015

Biology of Reproduction

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Vertebrate eggs are arrested at metaphase of meiosis II, a state classically known as cytostatic factor arrest. Maintenance of this arrest until the time of fertilization and then fertilization-induced exit from metaphase II are crucial for reproductive success. Another key aspect of this meiotic arrest and exit is regulation of the metaphase II spindle, which must be appropriately localized adjacent to the egg cortex during metaphase II and then progress into successful asymmetric cytokinesis to produce the second polar body. This study examined the mitogen-activated protein kinases MAPK3 and MAPK1 (also known as ERK1/2) as regulators of these two related aspects of mammalian egg biology, specifically testing whether this MAPK pathway affected myosin-II function and whether myosin-II perturbation would produce some of the same effects as MAPK pathway perturbation. Inhibition of the MEK1/2-MAPK pathway with U0126 leads to reduced levels of phosphorylated myosin-regulatory light chain (pMRLC) and causes a reduction in cortical tension, effects that are mimicked by treatment with the myosin light chain kinase (MLCK) inhibitor ML-7. These data indicate that one mechanism by which the MAPK pathway acts in eggs is by affecting myosin-II function. We further show that MAPK or MLCK inhibition induces loss of normal cortical spindle localization or parthenogenetic egg activation. This parthenogenesis is dependent on cytosolic and extracellular calcium and can be rescued by hyperloading eggs with zinc, suggesting that these effects of inhibition of MLCK or the MAPK pathway are linked with dysregulation of ion homeostasis.

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“…Various methods have been employed to induce artificial calcium oscillations in mammalian oocytes in vitro and thereby provoke oocyte activation and embryo development. Electrical pulses [18], calcium ionophore [19], and strontium [20] are typically used as parthenogenetic agents, and it has been demonstrated that electrical pulses and calcium ionophore generate a single calcium elevation, whereas multiple calcium oscillations are induced by normal fertilization or strontium [20]. Moreover, there is some evidence that procaine is able to disregulate cytoplasmic calcium rise(s) in female gametes.…”

Section: Introductionmentioning

confidence: 98%

Procaine Induces Cytokinesis in Horse Oocytes via a pH-Dependent Mechanism1

Leemans

Gadella

Stout

et al. 2015

Biology of Reproduction

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Coincubating equine gametes in the presence of procaine has been reported to facilitate in vitro fertilization, with cleavage rates exceeding 60%. We report that while procaine does trigger sperm hyperactivation, it independently induces cleavage of equine oocytes. First, we found that procaine (1-5 mM) did not facilitate stallion sperm penetration of equine oocytes but instead induced sperm-independent oocyte cytokinesis in the absence of the second polar body extrusion. Indeed, 56 ± 4% of oocytes cleaved within 2.5 days of exposure to 2.5 mM procaine regardless of sperm presence. However, the cleaved oocytes did not develop beyond 8 to 16 cells, and the daughter cells either lacked nuclei or contained aberrant, condensed DNA fragments. By contrast, intracytoplasmic sperm injection (ICSI) was followed by second polar body extrusion and formation of normal blastocysts. Moreover, neither the calcium oscillations detectable using fura-2 AM staining nor the cortical granule reaction visualized by LCA-FITC staining, after oocyte activation induced by ICSI or ionomycin treatment, were detected after exposing oocytes to 2.5 mM procaine. Instead, procaine initiated an ooplasmic alkalinization, detectable by BCECF-AM staining that was not observed after other treatments. This alkalinization was followed, after an additional 18 h of incubation, by cortical F-actin depolymerization, as demonstrated by reduced actin phalloidin-FITC staining intensity, that resembled preparation for cytokinesis in ICSI-fertilized zygotes. Overall, we conclude that procaine induces cytokinesis in equine oocytes accompanied by aberrant chromatin condensation and division; this explains why embryos produced after exposing equine oocytes to procaine fail to develop beyond the 8- to 16-cell stage.

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TRPV3 Channels Mediate Strontium-Induced Mouse-Egg Activation

Cited by 68 publications

References 79 publications

Store-operated Ca 2+ entry is not required for fertilization-induced Ca 2+ signaling in mouse eggs

Store-operated Ca 2+ entry is not required for fertilization-induced Ca 2+ signaling in mouse eggs

MAPK3/1 (ERK1/2) and Myosin Light Chain Kinase in Mammalian Eggs Affect Myosin-II Function and Regulate the Metaphase II State in a Calcium- and Zinc-Dependent Manner1

Procaine Induces Cytokinesis in Horse Oocytes via a pH-Dependent Mechanism1

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