人类胚胎的染色体挑战:机制和基础。

IF 3.3 Q2 GENETICS & HEREDITY
HGG Advances Pub Date : 2025-07-10 Epub Date: 2025-04-10 DOI:10.1016/j.xhgg.2025.100437
Anna Ivanova, Elena Korchivaia, Maria Semenova, Igor Lebedev, Ilya Mazunin, Ilya Volodyaev
{"title":"人类胚胎的染色体挑战:机制和基础。","authors":"Anna Ivanova, Elena Korchivaia, Maria Semenova, Igor Lebedev, Ilya Mazunin, Ilya Volodyaev","doi":"10.1016/j.xhgg.2025.100437","DOIUrl":null,"url":null,"abstract":"<p><p>Chromosomal abnormalities in human pre-implantation embryos, originating from either meiotic or mitotic errors, present a significant challenge in reproductive biology. Complete aneuploidy is primarily linked to errors during the resumption of meiosis in oocyte maturation, which increase with maternal age, while mosaic aneuploidies result from mitotic errors after fertilization. The biological causes of these abnormalities are increasingly becoming a topic of interest for research groups and clinical specialists. This review explores the intricate processes of meiotic and early mitotic divisions in embryos, shedding light on the mechanisms that lead to changes in chromosome number in daughter cells. Key factors in meiotic division include difficulties in spindle assembly without centrosomes, kinetochore (KT) orientation disturbances, and inefficient cell-cycle checkpoints. The weakening of cohesion molecules that bind chromosomes, exacerbated by maternal aging, further complicates chromosomal segregation. Mitotic errors in early development are influenced by defects in sperm centrosomes, KT misalignment, and the gradual depletion of maternal regulatory factors. Coupled with the inactive or partially active embryonic genome, this depletion increases the likelihood of chromosomal aberrations. While various theoretical mechanisms for these abnormalities exist, current data remain insufficient to determine their exact contributions. Continued research is essential to unravel these complex processes and improve outcomes in assisted reproductive technologies.</p>","PeriodicalId":34530,"journal":{"name":"HGG Advances","volume":"6 3","pages":"100437"},"PeriodicalIF":3.3000,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12050003/pdf/","citationCount":"0","resultStr":"{\"title\":\"The chromosomal challenge of human embryos: Mechanisms and fundamentals.\",\"authors\":\"Anna Ivanova, Elena Korchivaia, Maria Semenova, Igor Lebedev, Ilya Mazunin, Ilya Volodyaev\",\"doi\":\"10.1016/j.xhgg.2025.100437\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Chromosomal abnormalities in human pre-implantation embryos, originating from either meiotic or mitotic errors, present a significant challenge in reproductive biology. Complete aneuploidy is primarily linked to errors during the resumption of meiosis in oocyte maturation, which increase with maternal age, while mosaic aneuploidies result from mitotic errors after fertilization. The biological causes of these abnormalities are increasingly becoming a topic of interest for research groups and clinical specialists. This review explores the intricate processes of meiotic and early mitotic divisions in embryos, shedding light on the mechanisms that lead to changes in chromosome number in daughter cells. Key factors in meiotic division include difficulties in spindle assembly without centrosomes, kinetochore (KT) orientation disturbances, and inefficient cell-cycle checkpoints. The weakening of cohesion molecules that bind chromosomes, exacerbated by maternal aging, further complicates chromosomal segregation. Mitotic errors in early development are influenced by defects in sperm centrosomes, KT misalignment, and the gradual depletion of maternal regulatory factors. Coupled with the inactive or partially active embryonic genome, this depletion increases the likelihood of chromosomal aberrations. While various theoretical mechanisms for these abnormalities exist, current data remain insufficient to determine their exact contributions. Continued research is essential to unravel these complex processes and improve outcomes in assisted reproductive technologies.</p>\",\"PeriodicalId\":34530,\"journal\":{\"name\":\"HGG Advances\",\"volume\":\"6 3\",\"pages\":\"100437\"},\"PeriodicalIF\":3.3000,\"publicationDate\":\"2025-07-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12050003/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"HGG Advances\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1016/j.xhgg.2025.100437\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/4/10 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"HGG Advances","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1016/j.xhgg.2025.100437","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/4/10 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
引用次数: 0

摘要

人类着床前胚胎的染色体异常,起源于减数分裂或有丝分裂错误,在生殖生物学中提出了重大挑战。完全非整倍性主要与卵母细胞成熟过程中减数分裂恢复过程中的错误有关,这种错误随着母亲年龄的增长而增加,而花叶非整倍性则是受精后有丝分裂错误造成的。这些异常的生物学原因正日益成为研究小组和临床专家感兴趣的话题。这篇综述探讨了胚胎减数分裂和早期有丝分裂的复杂过程,揭示了导致子细胞染色体数目变化的机制。减数分裂的关键因素包括纺锤体在没有中心体的情况下组装困难,着丝点(KT)定向干扰和低效的细胞周期检查点。结合染色体的内聚力分子的减弱,再加上母亲的衰老,使染色体分离进一步复杂化。早期发育中的有丝分裂错误受精子中心体缺陷、KT错位和母体调节因子逐渐耗竭的影响。再加上不活跃或部分活跃的胚胎基因组,这种消耗增加了染色体畸变的可能性。虽然存在这些异常的各种理论机制,但目前的数据仍然不足以确定它们的确切贡献。持续的研究对于解开这些复杂的过程和改善辅助生殖技术的结果至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The chromosomal challenge of human embryos: Mechanisms and fundamentals.

Chromosomal abnormalities in human pre-implantation embryos, originating from either meiotic or mitotic errors, present a significant challenge in reproductive biology. Complete aneuploidy is primarily linked to errors during the resumption of meiosis in oocyte maturation, which increase with maternal age, while mosaic aneuploidies result from mitotic errors after fertilization. The biological causes of these abnormalities are increasingly becoming a topic of interest for research groups and clinical specialists. This review explores the intricate processes of meiotic and early mitotic divisions in embryos, shedding light on the mechanisms that lead to changes in chromosome number in daughter cells. Key factors in meiotic division include difficulties in spindle assembly without centrosomes, kinetochore (KT) orientation disturbances, and inefficient cell-cycle checkpoints. The weakening of cohesion molecules that bind chromosomes, exacerbated by maternal aging, further complicates chromosomal segregation. Mitotic errors in early development are influenced by defects in sperm centrosomes, KT misalignment, and the gradual depletion of maternal regulatory factors. Coupled with the inactive or partially active embryonic genome, this depletion increases the likelihood of chromosomal aberrations. While various theoretical mechanisms for these abnormalities exist, current data remain insufficient to determine their exact contributions. Continued research is essential to unravel these complex processes and improve outcomes in assisted reproductive technologies.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
HGG Advances
HGG Advances Biochemistry, Genetics and Molecular Biology-Molecular Medicine
CiteScore
4.30
自引率
4.50%
发文量
69
审稿时长
14 weeks
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信