Abstract
Rad51 is a conserved eukaryotic protein that mediates the homologous recombination repair of DNA double-strand breaks that occur during mitosis and meiosis. In addition, Rad51 promotes mitochondrial DNA synthesis when replication stress is increased. Rad51 also regulates cell cycle progression by preserving the G2/M transition in embryonic stem cells. In this study, we report a novel function of Rad51 in regulating mitochondrial activity during in vitro maturation of mouse oocytes. Suppression of Rad51 by injection of Rad51 dsRNA into germinal vesicle-stage oocytes resulted in arrest of meiosis in metaphase I. Rad51-depleted oocytes showed chromosome misalignment and failures in spindle aggregation, affecting the completion of cytokinesis. We found that Rad51 depletion was accompanied by decreased ATP production and mitochondrial membrane potential and increased DNA degradation. We further demonstrated that the mitochondrial defect activated autophagy in Rad51-depleted oocytes. Taken together, we concluded that Rad51 functions to safeguard mitochondrial integrity during the meiotic maturation of oocytes.
Highlights
The Metaphase II (MII) stage during in vitro maturation[17]
We report for the first time that Rad[51] regulates mitochondrial activity during in vitro maturation of mouse oocytes
We found that Rad[51] depletion led to reductions in ATP production, mitochondrial potential, and mitochondrial quantity in MI-stage oocytes, supporting a novel role of Rad[51] in the maintenance of mitochondrial dynamics and activity during the meiotic cell cycle in oocytes
Summary
The MII stage during in vitro maturation[17]. Another study focused on the role of Rad[51] in the meiotic maturation of undamaged oocytes[19]. The molecular mechanisms underlying Rad[51] activity during the meiotic maturation of oocytes remain to be elucidated. We report for the first time that Rad[51] regulates mitochondrial activity during in vitro maturation of mouse oocytes. Oocytes went into MI arrest following the suppression of Rad[51] during in vitro oocyte maturation. We found that Rad[51] depletion led to reductions in ATP production, mitochondrial potential, and mitochondrial quantity in MI-stage oocytes, supporting a novel role of Rad[51] in the maintenance of mitochondrial dynamics and activity during the meiotic cell cycle in oocytes
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