Haploid gametes, named oocytes and spermatozoa, are generated through two specialized cell divisions without intervening S-phase, from a diploid precursor cell. In the first division, named meiosis I, paired chromosomes are segregated and distributed into two daughter cells, whereas in meiosis II and mitosis, sister chromatids are segregated. Missegregations of the genetic material in meiosis have severe consequences, because they lead to the generation of aneuploid gametes (harboring the wrong number of chromosomes). In humans, meiosis is error prone, with an estimated 20 % of fertilizable oocytes being aneuploid. Trisomies, such as trisomy 21, are due to missegregations of a chromosome in meiosis. Furthermore, oocytes of women closer to menopause show a dramatic age-dependent increase in meiotic missegregations. Using ascidian and mouse oocytes we aim at elucidating the mechanisms of chromosome segregation during female meiosis to understand why it can go awry. We study how chromosomes are held together through a protein complex named Cohesin, which has to be removed in a two-step process during the two meiotic divisions. A pool of Cohesin is protected from removal in meiosis I, but not meiosis II. Whereas the mechanisms of Cohesin protection start to be better understood, its "deprotection" is largely unknown. We will determine how this "deprotection" in meiosis II takes place.