Abstract
The spindle assembly checkpoint suspends cell cycle progression if improperly aligned chromosomes are detected at metaphase. Evolutionarily conserved kinetochore-associated proteins are believed to be key elements of this regulatory pathway. A breakdown in checkpoint function could bring about genomic instability, which may be responsible for the prevalence of aneuploidy in oocytes of older women. Maternal aging remains the overwhelming factor in the etiology of human aneuploidy in assisted reproduction. Defects in cell cycle checkpoint genes may play a role in its development. The existence of such monitoring mechanisms in oocytes has long been controversial. Studies providing evidence in support of and against their existence are reviewed.