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Female gametogenesis (also referred to as oogenesis) is the process by which diploid (2n) cells undergo cell division through meiosis to form haploid (1n) gametes. A functional understanding of how these haploid cells form in the ovary provides insight into the pathologies arising from dysfunction during female gametogenesis. The following topic aims to discuss the cellular mechanisms behind the formation of haploid gametes, the role and function of haploid gametes formed by female gametogenesis, and the pathophysiology behind the outcomes of incorrect gametogenesis.[1]

Incorrect gametogenesis can lead to several pathologies, although an exhaustive discussion is not covered here. It is worth noting that aneuploidy is more common in female gametogenesis despite the higher rate of recombination also seen during female gametogenesis compared to gametogenesis in males. Errors resulting in aneuploidy, regardless of etiology, unsurprisingly, lead to fetal chromosomal abnormalities such as Down Syndrome as well as miscarriage and age-related infertility. Meiosis I, in particular, is associated with age-related increases in chromosomal missegregation. Although aneuploidy, in general, is most likely multi-factorial, the age-related decline in the presence of cohesive molecules holding chromosomes together during meiosis leads to a predisposition of becoming aneuploid via nondisjunction of homologous chromosomes. In rare instances, nutritional defects during the differentiation of oocytes can interfere with their fertilization, causing a hydatidiform mole leading to gestational trophoblastic disease.[1][8][9][10]