| First Author | Bernhardt ML | Year | 2017 |
| Journal | Cell Calcium | Volume | 65 |
| Pages | 63-72 | PubMed ID | 28222911 |
| Mgi Jnum | J:350391 | Mgi Id | MGI:7625820 |
| Doi | 10.1016/j.ceca.2017.02.004 | Citation | Bernhardt ML, et al. (2017) Store-operated Ca(2+) entry is not required for fertilization-induced Ca(2+) signaling in mouse eggs. Cell Calcium 65:63-72 |
| abstractText | Repetitive oscillations in cytoplasmic Ca(2+) due to periodic Ca(2+) release from the endoplasmic reticulum (ER) drive mammalian embryo development following fertilization. Influx of extracellular Ca(2+) to support the refilling of ER stores is required for sustained Ca(2+) oscillations, but the mechanisms underlying this Ca(2+) influx are controversial. Although store-operated Ca(2+) 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, Ca(2+) influx was assessed in oocytes and eggs lacking the major components of SOCE, the ER Ca(2+) sensor STIM proteins, and the plasma membrane Ca(2+) 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 Ca(2+) oscillations following fertilization. In addition, no impairment was observed in ER Ca(2+) stores or Ca(2+) influx following store depletion. Similar studies were performed on eggs from mice globally lacking ORAI1; no abnormalities were observed. Furthermore, spontaneous Ca(2+) influx was normal in oocytes from Stim1/2 cKO and ORAI1-null mice. Finally, we tested if TRPM7-like channels could support spontaneous Ca(2+) influx, and found that it was largely prevented by NS8593, a TRPM7-specific inhibitor. Fertilization-induced Ca(2+) oscillations were also impaired by NS8593. Combined, these data robustly show that SOCE is not required to support appropriate Ca(2+) signaling in mouse oocytes and eggs, and that TRPM7-like channels may contribute to Ca(2+) influx that was previously attributed to SOCE. |
