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Updated: Mar 8, 2026
Evaluation of the Spindle Assembly Checkpoint Integrity in Mouse Oocytes
Published on: September 13, 2022
Smc1β is required for activation of SAC during mouse oocyte meiosis
Yilong Miao1, Changyin Zhou1, Zhaokang Cui1
1a College of Animal Science and Technology, Nanjing Agricultural University , Nanjing , China.
Abstract:
Smc1β is a meiosis-specific cohesin subunit that is essential for sister chromatid cohesion and DNA recombination. Previous studies have shown that Smc1β-deficient mice in both sexes are sterile. Ablation of Smc1β during male meiosis leads to the blockage of spermatogenesis in pachytene stage, and ablation of Smc1β during female meiosis generates a highly error-prone oocyte although it could develop to metaphase II stage. However, the underlying mechanisms regarding how Smc1β maintains the correct meiotic progression in mouse oocytes have not been clearly defined. Here, we find that GFP-fused Smc1β is expressed and localized to the chromosomes from GV to MII stages during mouse oocyte meiotic maturation. Knockdown of Smc1β by microinjection of gene-specific morpholino causes the impaired spindle apparatus and chromosome alignment which are highly correlated with the defective kinetochore-microtubule attachments, consequently resulting in a prominently higher incidence of aneuploid eggs. In addition, the premature extrusion of polar bodies and escape of metaphase I arrest induced by low dose of nocodazole treatment in Smc1β-depleted oocytes indicates that Smc1β is essential for activation of spindle assembly checkpoint (SAC) activity. Collectively, we identify a novel function of Smc1β as a SAC participant beyond its role in chromosome cohesion during mouse oocyte meiosis.
Insights
Smc1β is crucial for mouse oocyte meiosis, ensuring proper chromosome alignment and spindle assembly checkpoint (SAC) function. Its absence leads to aneuploidy and developmental errors.
Area of Science:
- Cell Biology
- Genetics
- Reproductive Biology
Background:
- Smc1β is a meiosis-specific cohesin subunit vital for sister chromatid cohesion and DNA recombination.
- Smc1β deficiency in mice causes sterility, with spermatogenesis arrest in males and error-prone oocytes in females.
- The precise role of Smc1β in maintaining correct meiotic progression in oocytes remains unclear.
Purpose of the Study:
- To elucidate the underlying mechanisms of Smc1β's role in mouse oocyte meiotic progression.
- To investigate Smc1β's function beyond chromosome cohesion during oocyte meiosis.
Main Methods:
- Tracking GFP-tagged Smc1β expression and localization during oocyte maturation (GV to MII stages).
- Gene knockdown of Smc1β using microinjected morpholinos.
- Assessing spindle apparatus, chromosome alignment, kinetochore-microtubule attachments, and aneuploidy incidence.
- Evaluating spindle assembly checkpoint (SAC) activity via nocodazole treatment and polar body extrusion.
Main Results:
- Smc1β is expressed and localized to chromosomes throughout mouse oocyte meiotic maturation.
- Smc1β knockdown results in impaired spindle apparatus, chromosome misalignment, and defective kinetochore-microtubule attachments.
- Depletion of Smc1β significantly increases aneuploid egg incidence.
- Smc1β-depleted oocytes show premature polar body extrusion and escape metaphase I arrest, indicating compromised SAC activity.
Conclusions:
- Smc1β is essential for proper spindle formation, chromosome alignment, and kinetochore-microtubule attachments in mouse oocytes.
- Smc1β plays a critical role in the activation and function of the spindle assembly checkpoint (SAC) during oocyte meiosis.
- This study identifies a novel function for Smc1β as a SAC participant, extending its known role in chromosome cohesion.
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