SMC1beta-deficient female mice provide evidence that cohesins are a missing link in age-related nondisjunction

Research output: Contribution to journalResearch articleContributedpeer-review


  • Craig A Hodges - , Case Western Reserve University (Author)
  • Ekaterina Revenkova - (Author)
  • Rolf Jessberger - , Institute of Physiological Chemistry (Author)
  • Terry J Hassold - (Author)
  • Patricia A Hunt - (Author)


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.


Original languageEnglish
Pages (from-to)1351-5
Number of pages5
JournalNature genetics
Issue number12
Publication statusPublished - Dec 2005



  • Age Factors, Aneuploidy, Animals, Cell Cycle Proteins/genetics, Chromosomes/metabolism, Female, Meiosis/genetics, Mice, Nondisjunction, Genetic, Oocytes/cytology, Oogenesis/genetics