SMC1beta-deficient female mice provide evidence that cohesins are a missing link in age-related nondisjunction
Research output: Contribution to journal › Research article › Contributed › peer-review
Contributors
Abstract
Mitotic chromosome segregation is facilitated by the cohesin complex, which maintains physical connections between sister chromatids until anaphase. Meiotic cell division is considerably more complex, as cohesion must be released sequentially to facilitate orderly segregation of chromosomes at both meiosis I and meiosis II. This necessitates meiosis-specific cohesin components; recent studies in rodents suggest that these influence chromosome behavior during both cell division and meiotic prophase. To elucidate the role of the meiosis-specific cohesin SMC1beta (encoded by Smc1l2) in oogenesis, we carried out meiotic studies of female SMC1beta-deficient mice. Our results provide the first direct evidence that SMC1beta acts as a chiasma binder in mammals, stabilizing sites of exchange until anaphase. Additionally, our observations support the hypothesis that deficient cohesion is an underlying cause of human age-related aneuploidy.
Details
Original language | English |
---|---|
Pages (from-to) | 1351-1355 |
Number of pages | 5 |
Journal | Nature genetics |
Volume | 37 |
Issue number | 12 |
Publication status | Published - Dec 2005 |
Peer-reviewed | Yes |
External IDs
Scopus | 28444461450 |
---|
Keywords
Keywords
- Age Factors, Aneuploidy, Animals, Cell Cycle Proteins/genetics, Chromosomes/metabolism, Female, Meiosis/genetics, Mice, Nondisjunction, Genetic, Oocytes/cytology, Oogenesis/genetics