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Parthenogenetic activation of oocytes in c-mos-deficient mice
N Hashimoto1, N Watanabe, Y Furuta
1Mitsubishi Kasei Institute of Life Sciences, Tokyo, Japan.
Abstract:
In Xenopus the c-mos proto-oncogene product (Mos) is essential for the initiation of oocyte maturation, for the progression from meiosis I to meiosis II and for the second meiotic metaphase arrest, acting as an essential component of the cytostatic factor CSF. Its function in mouse oocytes is unclear, however, as is the biological significance of c-mos mRNA expression in testes and several somatic tissues. We have generated c-mos-deficient mice by gene targeting in embryonic stem cells. These mice grew at the same rate as their wild-type counterparts and reproduction was normal in the males, but the fertility of the females was very low. The c-mos-deficient female mice developed ovarian teratomas at a high frequency. Oocytes from these females matured to the second meiotic metaphase both in vivo and in vitro, but were activated without fertilization. The results indicate that in mice Mos plays a role in the second meiotic metaphase arrest, but does not seem to be essential for the initiation of oocyte maturation, spermatogenesis or somatic cell cycle.
Insights
The c-mos proto-oncogene is crucial for mouse oocyte maturation arrest but not initiation. C-mos-deficient female mice show low fertility and ovarian teratomas, indicating Mos
Area of Science:
- Developmental Biology
- Molecular Biology
- Oncology
Background:
- The c-mos proto-oncogene product (Mos) is vital for oocyte maturation and meiotic arrest in Xenopus.
- The precise role and biological significance of Mos in mouse oocytes, testes, and somatic tissues remain largely undetermined.
- Understanding Mos function is critical for comprehending cell cycle regulation and potential oncogenic pathways.
Purpose of the Study:
- To investigate the function of Mos in mouse oocyte maturation and meiotic arrest.
- To determine the biological significance of c-mos expression in mouse reproduction and somatic tissues.
- To generate and characterize c-mos-deficient mice to elucidate Mos roles in vivo.
Main Methods:
- Gene targeting in embryonic stem cells to create c-mos-deficient mice.
- Phenotypic analysis of c-mos-deficient mice, including growth, reproduction, and tumor development.
- In vivo and in vitro assessment of oocyte maturation and meiotic progression in deficient females.
Main Results:
- C-mos-deficient female mice exhibited significantly reduced fertility and a high incidence of ovarian teratomas.
- Oocytes from deficient females underwent maturation to the second meiotic metaphase but activated spontaneously without fertilization.
- Male mice and somatic tissues showed no apparent defects, suggesting a specific role for Mos in female meiosis.
Conclusions:
- Mos plays a critical role in maintaining the second meiotic metaphase arrest in mouse oocytes.
- Mos is not essential for the initiation of oocyte maturation, spermatogenesis, or somatic cell cycle progression in mice.
- The absence of Mos leads to parthenogenetic activation and teratoma formation, highlighting its importance in preventing aberrant oocyte development.