The effect is chromosome specific, as centromeric cohesin shapes kinetochore structure to promote efficient MCC production in meiosis I. A crucial implication for aging oocytes is that cohesin deterioration compromises the SAC in two ways: by promoting sister kinetochore biorientation and by impairing efficient MCC production at kinetochores that have not come under tension, thereby leading to meiosis I chromosome segregation errors such as those underlying trisomy 21 or Down’s syndrome. This evidence concerns the gene ADCY10 and Down syndrome.