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Transcriptional status of mouse oocytes corresponds with their ability to generate Ca2+ release.

In fully grown ovarian follicles both transcriptionally active (NSN) and inactive (SN) oocytes are present. NSN oocytes have been shown to display lower developmental potential. It is possible that oocytes that have not completed transcription before meiosis resumption accumulate less RNA and proteins required for their further development, including those responsible for regulation of Ca2+ homeostasis. Oscillations of the cytoplasmic concentration of free Ca2+ ions ([Ca2+]i) are triggered in oocytes by a fertilizing spermatozoon and are crucial for inducing and regulating further embryonic development. We showed that NSN-derived oocytes express less inositol 1,4,5-triphosphate receptor type 1 (IP3R1), store less Ca2+ ions, and generate weaker spontaneous [Ca2+]i oscillations during maturation than SN oocytes. Consequently, NSN oocytes display aberrant [Ca2+]i oscillations at fertilization. We speculate that this defective regulation of Ca2+ homeostasis might be one of the factors responsible for the lower developmental potential of NSN oocytes.