
Is age‐related increase of chromosome segregation errors in mammalian oocytes caused by cohesin deterioration?
Author(s) -
Lee Jibak
Publication year - 2020
Publication title -
reproductive medicine and biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.005
H-Index - 22
eISSN - 1447-0578
pISSN - 1445-5781
DOI - 10.1002/rmb2.12299
Subject(s) - cohesin , establishment of sister chromatid cohesion , chromosome segregation , meiosis , biology , sister chromatids , microbiology and biotechnology , genetics , meiosis ii , kinetochore , mitosis , homologous chromosome , chromosome , gene
Background Mammalian oocytes initiate meiosis in fetal ovary and are arrested at dictyate stage in prophase I for a long period. It is known that incidence of chromosome segregation errors in oocytes increases with advancing age, but the molecular mechanism underlying this phenomenon has not been clarified. Methods Cohesin, a multi‐subunit protein complex, mediates sister chromatid cohesion in both mitosis and meiosis. In this review, molecular basis of meiotic chromosome cohesion and segregation is summarized. Further, the relationship between chromosome segregation errors and cohesin deterioration in aged oocytes is discussed. Results Recent studies show that chromosome‐associated cohesin decreases in an age‐dependent manner in mouse oocytes. Furthermore, conditional knockout or activation of cohesin in oocytes indicates that only the cohesin expressed before premeiotic S phase can establish and maintain sister chromatic cohesion and that cohesin does not turnover during the dictyate arrest. Conclusion In mice, the accumulating evidence suggests that deterioration of cohesin due to the lack of turnover during dictyate arrest is one of the major causes of chromosome segregation errors in aged oocytes. However, whether the same is true in human remains elusive since even the deterioration of cohesin during dictyate arrest has not been demonstrated in human oocytes.