Regulation of store-operated Ca2+ entry during the cell cycle

Arredouani, Abdelilah; Yu, Fang; Sun, Lu; Machaca, Khaled

doi:10.1242/jcs.069690

Cited by 27 publications

(22 citation statements)

References 136 publications

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“…Although some Ca 2+ influx via SOCE channels probably occurs during egg activation, it is not likely to be required based on our findings that two different SOCE inhibitors could not block Ca 2+ oscillations or egg activation in response to sperm. This finding is consistent with previous observations that SOCE is inactivated during meiosis in Xenopus oocytes (27,28). Instead, our data suggest that one or more alternate Ca 2+ -permeable channels are opened in response to the initial Ca 2+ sensitization or indirectly in response to an activated signaling cascade, (e.g., one involving PLC or PKC activation).…”

Section: Discussionsupporting

confidence: 93%

Calcium influx-mediated signaling is required for complete mouse egg activation

Miao

Stein

Jefferson

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

130

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Mammalian fertilization is accompanied by oscillations in egg cytoplasmic calcium (Ca(2+)) concentrations that are critical for completion of egg activation. These oscillations are initiated by Ca(2+) release from inositol 1,4,5-trisphosphate (IP(3))-sensitive intracellular stores. We tested the hypothesis that Ca(2+) influx across the plasma membrane was a requisite component of egg activation signaling, and not simply a Ca(2+) source for store repletion. Using intracytoplasmic sperm injection (ICSI) and standard in vitro fertilization (IVF), we found that Ca(2+) influx was not required to initiate resumption of meiosis II. However, even if multiple oscillations in intracellular Ca(2+) occurred, in the absence of Ca(2+) influx, the fertilized eggs failed to emit the second polar body, resulting in formation of three pronuclei. Additional experiments using the Ca(2+) chelator, BAPTA/AM, demonstrated that Ca(2+) influx is sufficient to support polar body emission and pronucleus formation after only a single sperm-induced Ca(2+) transient, whereas BAPTA/AM-treated ICSI or fertilized eggs cultured in Ca(2+)-free medium remained arrested in metaphase II. Inhibition of store-operated Ca(2+) entry had no effect on ICSI-induced egg activation, so Ca(2+) influx through alternative channels must participate in egg activation signaling. Ca(2+) influx appears to be upstream of CaMKIIγ activity because eggs can be parthenogenetically activated with a constitutively active form of CaMKIIγ in the absence of extracellular Ca(2+). These results suggest that Ca(2+) influx at fertilization not only maintains Ca(2+) oscillations by replenishing Ca(2+) stores, but also activates critical signaling pathways upstream of CaMKIIγ that are required for second polar body emission.

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Section: Discussionsupporting

confidence: 93%

Calcium influx-mediated signaling is required for complete mouse egg activation

Miao

Stein

Jefferson

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

130

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“…In a similar fashion to what is observed during Xenopus meiosis, SOCE inactivates fully during mitosis of mammalian cells (Arredouani et al, 2010;Preston et al, 1991;Tani et al, 2007). Therefore, SOCE inactivates during both meiosis and mitosis, with the only exception being mammalian oocyte meiosis during which SOCE activity can still be detected.…”

Section: Introductionsupporting

confidence: 72%

“…SOCE has been shown to be consistently downregulated during cell division (Arredouani et al, 2010), however the significance of this inhibition remained unclear. Here we show that SOCE levels in the mature MII egg modulate the periodicity and duration of Ca 2+ oscillations and the duration of the Ca 2+ signal at egg activation.…”

Section: Discussionmentioning

confidence: 99%

Down-regulation of store-operated Ca2+ entry during mammalian meiosis is required for the egg-to-embryo transition

Lee

Palermo

Machaca

2013

Journal of Cell Science

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SummaryA specialized Ca 2+ transient at fertilization represents the universal driver for the egg-to-embryo transition. Ca 2+ signaling remodels during oocyte maturation to endow the egg with the capacity to produce the specialized Ca 2+ transient at fertilization, which takes the form of a single (e.g. Xenopus) or multiple (e.g. mouse) Ca 2+ spikes depending on the species. Store-operated Ca 2+ entry (SOCE) is the predominant Ca 2+ influx pathway in vertebrate oocytes, and in Xenopus SOCE completely inactivates during meiosis. Here, we show that SOCE is downregulated during mouse meiosis, but remains active in mature metaphase II eggs. SOCE inhibition is due to a decreased ability of the Ca 2+ sensor STIM1 to translocate to the cortical endoplasmic reticulum domain and due to internalization of Orai1. Reversing SOCE downregulation by overexpression of STIM1 and Orai1 prolongs the Ca 2+ oscillations at egg activation and disrupts the egg-to-embryo transition. Thus, SOCE downregulation during mammalian oocyte maturation is a crucial determinant of the fertilization-specific Ca 2+ transient, egg activation and early embryonic development.

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“…SOCE inactivation requires MPF activity [135]. Although speculative at this point, SOCE inactivation may prevent maverick Ca 2+ signals during cellular division that may interfere with normal cell division especially given the potential role of Ca 2+ signals during M-phase as discussed in details above [136]. SOCE inactivation was recently shown to be due to both internalization of the Orai1 channel and the inability of STIM1 to form clusters in response to store depletion in oocytes [137;138].…”

Section: Ca 2+ Signals Induce Cell Cycle Reentry Of Quiescent T-cmentioning

confidence: 99%

Ca2+ signaling, genes and the cell cycle

Machaca

2011

Cell Calcium

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Changes in the concentration and spatial distribution of Ca 2+ ions in the cytoplasm constitute a ubiquitous intracellular signaling module in cellular physiology. With the advent of Ca 2+ dyes that allow direct visualization of Ca 2+ transients, combined with powerful experimental tools such as electrophysiological recordings, intracellular Ca 2+ transients have been implicated in practically every aspect of cellular physiology, including cellular proliferation. Ca 2+ signals are associated with different phases of the cell cycle and interfering with Ca 2+ signaling or downstream pathways often disrupts progression of the cell cycle. Although there exists a dependence between Ca 2+ signals and the cell cycle the mechanisms involved are not well defined and given the cross-talk between Ca 2+ and other signaling modules, it is difficult to assess the exact role of Ca 2+ signals in cell cycle progression. Two exceptions however, include fertilization and T-cell activation, where well-defined roles for Ca 2+ signals in mediating progression through specific stages of the cell cycle have been clearly established. In the case of T-cell activation Ca 2+ regulates entry into the cell cycle through the induction of gene transcription.

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Regulation of store-operated Ca2+ entry during the cell cycle

Cited by 27 publications

References 136 publications

Calcium influx-mediated signaling is required for complete mouse egg activation

Calcium influx-mediated signaling is required for complete mouse egg activation

Down-regulation of store-operated Ca2+ entry during mammalian meiosis is required for the egg-to-embryo transition

Ca2+ signaling, genes and the cell cycle

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