Oocyte is arrested at metaphase of the second meiosis until fertilization switching on [Ca]i oscillations. Oocyte activation inefficiency is the most challenging problem for failed fertilization and embryonic development. Mitochondrial function and intracellular [Ca]i oscillations are two critical factors for the oocyte's developmental potential. We aimed to understand the possible correlation between mitochondrial function and [Ca]i oscillations in oocytes. To this end, mitochondrial uncoupler CCCP which damages mitochondrial function and two small molecule mitochondrial agonists, L-carnitine (LC) and BGP-15, were used to examine the regulation of [Ca]i by mitochondrial functions. With increasing CCCP concentrations, [Ca]i oscillations were gradually diminished and high concentrations of CCCP led to oocyte death. LC enhanced mitochondrial membrane potential and [Ca]i oscillations and even improved the damage induced by CCCP, however, BGP-15 had no beneficial effect on oocyte activation. We have found that mitochondrial function plays a vital role in the generation of [Ca]i oscillations in oocytes, and thus mitochondria may interact with the ER to generate [Ca]i oscillations during oocyte activation. Improvement of mitochondrial functions with small molecules can be expected to improve oocyte activation and embryonic development in infertile patients without invasive micromanipulation.
Rab GTPases have multiple regulatory functions in intracellular vesicle transport. In recent years, there has been an increasing interest in the roles of Rab proteins in mammalian oocytes. In this paper, we show the specific distribution pattern of Rab24 during mouse oocyte meiosis. Furthermore, we find that Rab24 depletion results in the failure of maturational progression in mouse oocytes. Notably, the frequency of meiotic apparatus abnormality is significantly increased in Rab24-depleted oocytes relative to controls. In addition, lagging chromosomes are readily observed in anaphase/telophase oocytes with Rab24 knockdown. In support of this, the depletion of Rab24 disturbs the kinetochore-microtubule attachments in oocytes, and contributes to the production of aneuploid eggs. Taken together, the results of this study identify Rab24 as a novel factor in the modulation of meiotic apparatus assembly and meiotic progression during mouse oocyte maturation.
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