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Updated: Jun 24, 2026

Meiotic Spindle Assessment in Mouse Oocytes by siRNA-mediated Silencing
Published on: October 11, 2015
Spindle assembly checkpoint-related failure perturbs early embryonic divisions and reduces reproductive performance
Zuzanna Maciejewska1, Zbigniew Polanski, Katarzyna Kisiel
1Department of Embryology, Institute of Zoology, Faculty of Biology, University of Warsaw, Warsaw, Poland.
Abstract:
The phenotype of the LT/Sv strain of mice is manifested by abnormalities in oocyte meiotic cell-cycle, spontaneous parthenogenetic activation, teratomas formation, and frequent occurrence of embryonic triploidy. These abnormalities lead to the low rate of reproductive success. Recently, metaphase I arrest of LT/Sv oocytes has been attributed to the inability to timely inactivate the spindle assembly checkpoint (SAC). As differences in meiotic and mitotic SAC functioning were described, it remains obscure whether this abnormality is limited to the meiosis or also impinges on the mitotic divisions of LT/Sv embryos. Here, we show that a failure to inactivate SAC affects mitoses during preimplantation development of LT/Sv embryos. This is manifested by the prolonged localization of MAD2L1 on kinetochores of mitotic chromosomes and abnormally lengthened early embryonic M-phases. Moreover, LT/Sv embryos exhibit elevated frequency of abnormal chromosome separation during the first mitotic division. These abnormalities participate in severe impairment of preimplantation development and significantly decrease the reproductive success of this strain of mice. Thus, the common meiosis and mitosis SAC-related failure participates in a complex LT/Sv phenotype.
Insights
A spindle assembly checkpoint (SAC) failure impacts both meiosis and mitosis in LT/Sv mouse embryos, causing developmental defects and low reproductive success. This SAC dysfunction contributes to the complex LT/Sv phenotype.
Area of Science:
- Reproductive biology
- Developmental biology
- Cell cycle regulation
Background:
- LT/Sv mice exhibit reproductive issues including oocyte abnormalities, parthenogenesis, teratomas, and triploidy.
- Oocyte metaphase I arrest in LT/Sv mice is linked to delayed spindle assembly checkpoint (SAC) inactivation.
- The impact of SAC dysfunction on mitotic divisions in LT/Sv embryos is not well understood.
Purpose of the Study:
- To investigate whether the SAC inactivation defect in LT/Sv mice affects mitotic divisions during early embryonic development.
- To determine the consequences of SAC-related failures on preimplantation development in LT/Sv embryos.
Main Methods:
- Analysis of spindle assembly checkpoint (SAC) component localization (MAD2L1) on mitotic chromosomes in LT/Sv embryos.
- Assessment of embryonic M-phase duration during preimplantation development.
- Evaluation of chromosome segregation accuracy in the first mitotic division of LT/Sv embryos.
Main Results:
- Failure to inactivate SAC affects mitosis in LT/Sv embryos, evidenced by prolonged MAD2L1 kinetochore localization.
- LT/Sv embryos display abnormally lengthened early embryonic M-phases.
- Increased frequency of abnormal chromosome separation occurs during the first mitotic division in LT/Sv embryos.
- These mitotic abnormalities contribute to impaired preimplantation development and reduced reproductive success.
Conclusions:
- A common SAC-related failure affects both meiosis and mitosis in LT/Sv mice.
- This dual-action SAC defect is a significant contributor to the complex LT/Sv phenotype and reproductive failure.
- Understanding SAC function in both meiotic and mitotic divisions is crucial for addressing reproductive issues in this mouse model.
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