Abstract
Sister chromatid cohesion is essential for cell division. During meiosis, it is also required for proper synapsis of pairs of sister chromatids and for chiasma formation and maintenance. Since mammalian oocytes remain arrested in late prophase for a very long period—up to five decades in humans—the preservation of cohesion throughout this period is a formidable challenge. Mouse models with cohesin deficiencies and aging wild-type mice showed that this challenge is not fully met: cohesion weakens and deteriorates with increasing age. These recent findings have highly significant implications for our comprehension of the genesis of aneuploidies.
Highlights
To clarify whether Smc1α is expressed in oocytes after birth, we evaluated the relative amount of
If slow deterioration of cohesin is a major cause for mis-segregation in oocytes, one may expect to see a decrease in cohesion with age even in wild-type mice
If one assumes that sister chromatid cohesion relies solely on the cohesin loaded at the initial stages of meiosis, slow protein degradation may deplete cohesin from chromosomes
Summary
The SMC1β-based cohesin complex is present in mouse spermatocytes and oocytes throughout meiosis up to the metaphase/anaphase II transition [8]. SMC1β deficiency causes complete loss of sister chromatid cohesion in metaphase II as observed in Loss of cohesion with increasing age, like in female Smc1β-/- mice, may contribute to increased aneuploidy in ageing human oocytes.
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