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

Publikation: Beitrag in FachzeitschriftForschungsartikelBeigetragenBegutachtung

Beitragende

  • Craig A Hodges - , Case Western Reserve University (Autor:in)
  • Ekaterina Revenkova - (Autor:in)
  • Rolf Jessberger - , Institut für Physiologische Chemie (Autor:in)
  • Terry J Hassold - (Autor:in)
  • Patricia A Hunt - (Autor:in)

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

OriginalspracheEnglisch
Seiten (von - bis)1351-5
Seitenumfang5
FachzeitschriftNature genetics
Jahrgang37
Ausgabenummer12
PublikationsstatusVeröffentlicht - Dez. 2005
Peer-Review-StatusJa

Schlagworte

Schlagwörter

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