SMC1β-deficient female mice provide evidence that cohesins are a missing link in age-related nondisjunction

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(1,2). To elucidate the role of the meiosis-specific cohesin SMC1 beta ( encoded by Smc1l2) in oogenesis, we carried out meiotic studies of female SMC1 beta-deficient mice. Our results provide the first direct evidence that SMC1 beta 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.