Deterioration without replenishment--the misery of oocyte cohesin

Abstract

Humans suffer a steep increase in aneuploidies when oocytes age, and deterioration of cohesin was suggested recently as a prominent cause. In the November 15, 2010, issue of Genes & Development, Tachibana-Konwalski and colleagues (pp. 2505-2516) answered a question central to this hypothesis: Can cohesin be reloaded onto mouse oocyte chromosomes long after birth? They found that it cannot, or at least not with an efficiency adequate to rescue cohesin deficiency. With no chance for sufficient replenishment, age-related loss of sister chromatid cohesion seems unavoidable.

Figure 1.

Summary of oocyte development, cohesin status, and aneuploidies. (Top) Stages of human and mouse life are correlated with phases of meiosis, the status of cohesin, and the level of aneuploidies. A red triangle illustrates the rapid increase in aneuploidies during human female aging, particularly beyond 35 yr of age. Timing of embryonic prophase I, puberty, and menopause is approximate, and, in mice, depends on the particular mouse strain. The exact timing of onset of expression of each individual cohesin protein has not yet been determined, but indications exist for post-replicative loading of some cohesin in early prophase I. It is also unknown when after or even before birth cohesin deterioration starts. (Gestat. wk.) Gestational week; (e.d.) embryonic day.