Physiological and pathological mechanisms of oocyte meiosis.

Q3 Medicine 遗传 Pub Date : 2023-12-20 DOI:10.16288/j.yczz.23-170
Zhou Zhou, Qing Sang, Lei Wang
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Abstract

Normal oogenesis is crucial to successful reproduction. During the human female fetal stage, primordial germ cells transform from mitosis to meiosis. After synapsis and recombination of homologous chromosomes, meiosis is arrested at the diplotene stage of prophase in meiosis I. The maintenance of oocyte meiotic arrest in the follicle is primarily attributed to high cytoplasmic concentrations of cyclic adenosine monophosphate. During the menstrual cycle, follicle-stimulating hormone and luteinizing hormone lead to the resumption of meiosis that occurs in certain oocytes and complete the ovulation process. Anything that disturbs oocyte meiosis may result in failure of oogenesis and seriously affect both the fertilization and embryonic development. The rapid development of the assisted reproduction technology, high-throughput sequencing technology, and molecular biology technology provide new ideas and means for human to understand molecular mechanism of meiosis and diagnosis and treatment of oocyte maturation defects. In this review, we mainly summarize the recent physiological and pathological mechanisms of oogenesis, involving homologous recombination, meiotic arrest and resumption, maternal mRNA degradation, post-translational regulation, zona pellucida assembly, and so on. We wish to take this opportunity to raise the awareness of researchers in related fields on oocyte meiosis, providing a theoretical basis for further research and disease treatments.

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卵母细胞减数分裂的生理和病理机制。
正常的卵子生成是成功繁殖的关键。在人类女性胎儿阶段,原始生殖细胞从有丝分裂转变为减数分裂。同源染色体经过突触和重组后,减数分裂停滞在减数分裂Ⅰ前期的二分裂阶段。卵泡中卵母细胞减数分裂停滞的维持主要归因于细胞质中高含量的环磷酸腺苷。在月经周期中,卵泡刺激素和黄体生成素会导致某些卵母细胞的减数分裂恢复,并完成排卵过程。任何干扰卵母细胞减数分裂的因素都可能导致卵子生成失败,严重影响受精和胚胎发育。辅助生殖技术、高通量测序技术和分子生物学技术的飞速发展,为人类认识减数分裂的分子机制、诊断和治疗卵母细胞成熟缺陷提供了新的思路和手段。在这篇综述中,我们主要总结了近年来卵母细胞发生的生理和病理机制,涉及同源重组、减数分裂停止和恢复、母体mRNA降解、翻译后调控、透明带组装等。我们希望借此机会提高相关领域研究人员对卵母细胞减数分裂的认识,为进一步的研究和疾病治疗提供理论依据。
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来源期刊
遗传
遗传 Medicine-Medicine (all)
CiteScore
2.50
自引率
0.00%
发文量
6699
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