A hypothesis: Could telomere length and/or epigenetic alterations contribute to infertility in females with Turner syndrome?

One of the traits most consistently seen in females with Turner syndrome is premature ovarian insufficiency (POI). The biological mechanisms underlying the germ cell atresia that leads to infertility in most women with Turner syndrome are unclear. Given that telomeres are important for proper chromosomal pairing and other early steps in meiosis and oogenesis, one can conjecture that perturbations in telomere length and/or function might contribute to the POI associated with Turner syndrome. Also, one can speculate that epigenetic modifications that arise in response to asynapsis, as well as the resetting of the epigenome during embryogenesis, could contribute to monosomy X-related germ cell atresia. Moreover, errors in recombination-based DNA repair might contribute to the failure of cells lacking all, or a portion of, a second sex chromosome to successfully complete oogenesis. This article presents a review of the extant literature related to telomere length and/or epigenetic patterns associated with POI in females with a monosomy X complement (in humans and animal models). A goal of this review is to inspire researchers to use new technological advances to better characterize the components of the biological cascade leading to early germ cell loss in females with Turner syndrome.