Current Biology
Volume 20, Issue 17, 14 September 2010, Pages 1529-1533
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Oocyte Cohesin Expression Restricted to Predictyate Stages Provides Full Fertility and Prevents Aneuploidy

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Summary

To ensure correct meiotic chromosome segregation, sister chromatid cohesion (SCC) needs to be maintained from its establishment in prophase I oocytes before birth until continuation of meiosis into metaphase II upon oocyte maturation in the adult. Aging human oocytes suffer a steep increase in chromosome missegregation and aneuploidy, which may be caused by loss of SCC through slow deterioration of cohesin [1, 2, 3]. This hypothesis assumes that cohesin expression in embryonic oocytes is sufficient to provide adequate long-term SCC. With increasing age, mouse oocytes deficient in the meiosis-specific cohesin SMC1β massively lose SCC and chiasmata [3, 4]. To test the deterioration hypothesis, we specifically and highly efficiently inactivated the mouse Smc1β gene at the primordial follicle stage shortly after birth, when oocytes had just entered meiosis I dictyate arrest. In the adult, however, irrespective of oocyte age, chiasma positions and SCC are normal. Frequency and size of litters prove full fertility even in aged females. Thus, SMC1β cohesin needs only be expressed during prophase I prior to the primordial follicle stage to ensure SCC up to advanced age of mice.

Highlights

► SMC1β cohesin is required for mammalian oocyte sister chromatid cohesion ► Prenatal SMC1β cohesin suffices for oocyte sister chromatid cohesion ► Postnatal cohesin is not required to prevent loss of oocyte chiasmata and aneuploidy ► No age-dependent loss of cohesion or chiasmata upon postnatal depletion of SMC1β

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