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Disruption of c-mos causes parthenogenetic development of unfertilized mouse eggs
W H Colledge1, M B Carlton, G B Udy
1Wellcome/CRC Institute of Cancer, University of Cambridge, UK.
Abstract:
The c-mos proto-oncogene encodes a 37-39K cytoplasmic serine/threonine kinase implicated in the meiotic maturation events during murine spermatogenesis and oogenesis. In Xenopus, ectopic expression of pp39mos can promote both the meiotic maturation of oocytes and also arrest the cleavage of blastomeres. To elucidate the role of pp39mos we have generated homozygous mutant mice by gene targeting in embryonic stem cells. These mice are viable and mutant males are fertile, demonstrating that pp39mos is not essential for spermatogenesis. In contrast, mutant females, have a reduced fertility because of the failure of mature eggs to arrest during meiosis. c-mos-/- oocytes undergo germinal vesicle breakdown and extrusion of both polar bodies followed in some cases by progression into cleavage. Mutant females also develop ovarian cysts. These results demonstrate that a major role for pp39mos is to prevent the spontaneous parthenogenetic activation of unfertilized eggs.
Insights
The c-mos proto-oncogene is not essential for male fertility but is crucial for female fertility. Mutant female mice lacking c-mos exhibit a failure to arrest eggs during meiosis, leading to reduced fertility.
Area of Science:
- Molecular Biology
- Developmental Biology
- Genetics
Background:
- The c-mos proto-oncogene encodes a serine/threonine kinase involved in meiotic maturation.
- In Xenopus, ectopic expression of pp39mos influences oocyte maturation and blastomere cleavage.
- The precise role of c-mos in mammalian reproduction requires elucidation.
Purpose of the Study:
- To investigate the essentiality of the c-mos proto-oncogene in murine spermatogenesis and oogenesis.
- To determine the function of pp39mos in regulating meiotic arrest and preventing parthenogenetic activation.
Main Methods:
- Gene targeting in embryonic stem cells to generate homozygous c-mos mutant mice.
- Phenotypic analysis of mutant mice, including fertility assessments and oocyte maturation studies.
Main Results:
- Homozygous c-mos mutant mice are viable, and mutant males are fertile, indicating c-mos is not essential for spermatogenesis.
- Mutant females display reduced fertility due to the failure of mature eggs to arrest during meiosis.
- c-mos-/- oocytes undergo germinal vesicle breakdown and polar body extrusion, with some progressing to cleavage.
- Mutant females develop ovarian cysts, suggesting broader reproductive system impacts.
Conclusions:
- The c-mos proto-oncogene plays a critical role in preventing the spontaneous parthenogenetic activation of unfertilized eggs in female mammals.
- pp39mos function is essential for maintaining meiotic arrest in mature oocytes, thereby ensuring female fertility.