Abstract: During meiosis, the female germ cells are prone to chromosomal separation errors, resulting in aneuploid oocytes. After fertilization, aneuploid embryos will be produced, resulting in birth defects or embryo death, which is an important factor affecting mammalian reproduction. Homologous chromosome synapsis occurs in oocytes at the early stage of the first meiosis, when DNA double strand breaks trigger recombination. The lack of crossover during recombination, the reduction of the number of recombination events and the proximity of crossover to telomeres or centromeres lead to co-oriented segregation or no segregation of chromosomes, then bringing about aneuploid oocytes. During meiosis, when there is an error in the connection between the chromosome kinetochore and the spindle microtuble, the spindle assembly checkpoint (spindle assembly checkpoint, SAC) is activated, the E3 ubiquitin ligase APC/Cyclome (APC/C) is silenced, and the APC targeting proteins securin and cyclin B are protected from degradation, thus inhibiting the separase and the continued separation of chromosomes. Until all chromosomes and spindles achieve stable bipolar orientation and are correctly arranged on the equatorial plate, SAC is closed and chromosomes are separated correctly. The absence of SAC protein in oocytes leads to SAC unable to effectively monitor the correct attachment of telomeres to the spindle, resulting in chromosome segregation errors and aneuploid oocytes. Therefore, analyzing the mechanism involved in aneuploid oocytes by modern molecular technology is an important goal to protect mammalian fertility. This article mainly introduced the characteristics of oocyte meiosis, and expounded in detail the molecular mechanism of chromosome segregation error in oocyte aneuploidy, in order to provide reference for the development of treatment methods for aneuploid oocytes.

Key words: oocyte; meiosis; aneuploidy; recombination; spindle assembly checkpoint (SAC)