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

Research output: Contribution to journalResearch articleContributedpeer-review

Contributors

  • Craig A Hodges - , Case Western Reserve University (Author)
  • Ekaterina Revenkova - , Icahn School of Medicine at Mount Sinai (Author)
  • Rolf Jessberger - , Institute of Physiological Chemistry, Icahn School of Medicine at Mount Sinai (Author)
  • Terry J Hassold - , Washington State University Pullman (Author)
  • Patricia A Hunt - , Washington State University Pullman (Author)

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 languageEnglish
Pages (from-to)1351-1355
Number of pages5
JournalNature genetics
Volume37
Issue number12
Publication statusPublished - Dec 2005
Peer-reviewedYes

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