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Overexpression of cyclin A1 promotes meiotic resumption but induces premature chromosome separation in mouse oocyte
- Source :
- Journal of Cellular Physiology. 235:7136-7145
- Publication Year :
- 2020
- Publisher :
- Wiley, 2020.
-
Abstract
- Mammalian cyclin A1 is prominently expressed in testis and essential for meiosis in the male mouse, however, it shows weak expression in ovary, especially during oocyte maturation. To understand why cyclin A1 behaves in this way in the oocyte, we investigated the effect of cyclin A1 overexpression on mouse oocyte meiotic maturation. Our results revealed that cyclin A1 overexpression triggered meiotic resumption even in the presence of germinal vesicle breakdown inhibitor, milrinone. Nevertheless, the cyclin A1-overexpressed oocytes failed to extrude the first polar body but were completely arrested at metaphase I. Consequently, cyclin A1 overexpression destroyed the spindle morphology and chromosome alignment by inducing premature separation of chromosomes and sister chromatids. Therefore, cyclin A1 overexpression will prevent oocyte maturation although it can promote meiotic resumption. All these results show that decreased expression of cyclin A1 in oocytes may have an evolutional significance to keep long-lasting prophase arrest and orderly chromosome separation during oocyte meiotic maturation.
- Subjects :
- 0301 basic medicine
Physiology
Clinical Biochemistry
Biology
Mice
03 medical and health sciences
Oogenesis
0302 clinical medicine
Prophase
Meiosis
Chromosome Segregation
medicine
Animals
Sister chromatids
RNA, Messenger
Chromosome separation
Separase
Cyclin
Mice, Inbred ICR
Germinal vesicle
Cell Biology
Oocyte
Up-Regulation
Cell biology
030104 developmental biology
medicine.anatomical_structure
030220 oncology & carcinogenesis
Oocytes
Female
Cyclin A1
Milrinone
Subjects
Details
- ISSN :
- 10974652 and 00219541
- Volume :
- 235
- Database :
- OpenAIRE
- Journal :
- Journal of Cellular Physiology
- Accession number :
- edsair.doi.dedup.....24370e25d1aa20dec8bced13840a2374
- Full Text :
- https://doi.org/10.1002/jcp.29612