Shanghai Ji Ai Genetics & IVF Institute, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, 200011, China.
Department of Obstetrics and Gynecology of Shanghai Medical School, Fudan University, Shanghai, 200032, China.
Reprod Biol Endocrinol. 2023 Oct 2;21(1):90. doi: 10.1186/s12958-023-01143-0.
In human female primordial germ cells, the transition from mitosis to meiosis begins from the fetal stage. In germ cells, meiosis is arrested at the diplotene stage of prophase in meiosis I (MI) after synapsis and recombination of homologous chromosomes, which cannot be segregated. Within the follicle, the maintenance of oocyte meiotic arrest is primarily attributed to high cytoplasmic concentrations of cyclic adenosine monophosphate (cAMP). Depending on the specific species, oocytes can remain arrested for extended periods of time, ranging from months to even years. During estrus phase in animals or the menstrual cycle in humans, the resumption of meiosis occurs in certain oocytes due to a surge of luteinizing hormone (LH) levels. Any factor interfering with this process may lead to impaired oocyte maturation, which in turn affects female reproductive function. Nevertheless, the precise molecular mechanisms underlying this phenomenon has not been systematically summarized yet. To provide a comprehensive understanding of the recently uncovered regulatory network involved in oocyte development and maturation, the progress of the cellular and molecular mechanisms of oocyte nuclear maturation including meiosis arrest and meiosis resumption is summarized. Additionally, the advancements in understanding the molecular cytoplasmic events occurring in oocytes, such as maternal mRNA degradation, posttranslational regulation, and organelle distribution associated with the quality of oocyte maturation, are reviewed. Therefore, understanding the pathways regulating oocyte meiotic arrest and resumption will provide detailed insight into female reproductive system and provide a theoretical basis for further research and potential approaches for novel disease treatments.
在人类女性原始生殖细胞中，从胎儿期开始就进入有丝分裂向减数分裂的转变。在生殖细胞中，同源染色体联会和重组后，减数分裂 I（MI）的前期双线期就会停滞，不能进行分离。在卵泡内，卵母细胞减数分裂停滞的维持主要归因于细胞质中环腺苷酸（cAMP）的高浓度。根据特定物种的不同，卵母细胞可以长时间（从几个月到甚至几年）保持停滞状态。在动物发情期或人类月经周期中，由于黄体生成素（LH）水平的激增，某些卵母细胞会重新开始减数分裂。任何干扰这个过程的因素都可能导致卵母细胞成熟受损，从而影响女性生殖功能。然而，目前尚未系统地总结出这种现象背后的精确分子机制。为了全面了解最近发现的与卵母细胞发育和成熟相关的调控网络，总结了卵母细胞核成熟包括减数分裂停滞和减数分裂恢复的细胞和分子机制的研究进展。此外，还综述了卵母细胞中细胞质事件的分子机制，如母体 mRNA 降解、翻译后调控和与卵母细胞成熟质量相关的细胞器分布等方面的研究进展。因此，了解调控卵母细胞减数分裂停滞和恢复的途径，将为女性生殖系统提供详细的认识，并为进一步的研究和潜在的新型疾病治疗方法提供理论基础。
