Conclusions
Taken together, our study demonstrated that exposure to NIV affected Cyclin B1 expression and activated microtubule stability-dependent SAC to ultimately disturb cell cycle progression in mouse oocyte meiosis.
Results
We set up a NIV exposure model and showed that NIV did not affect G2/M transition for meiosis resumption, but disrupted the polar body extrusion of oocytes. Further analysis revealed that oocytes were arrested at metaphase I, which might be due to the lower expression of Cyclin B1 after NIV exposure. After cold treatment, the microtubules were disassembled in the NIV-exposed oocytes, indicating that NIV disrupted microtubule stability. Moreover, NIV affected the attachment between kinetochore and microtubules, which further induced the activation of MAD2/BUBR1 at the kinetochores, suggesting that spindle assemble checkpoint (SAC) was continuously activated during oocyte meiotic maturation. Conclusions: Taken together, our study demonstrated that exposure to NIV affected Cyclin B1 expression and activated microtubule stability-dependent SAC to ultimately disturb cell cycle progression in mouse oocyte meiosis.