减数分裂是表观遗传学重编程和细胞年轻化的一种机制。

IF 3.7 2区 生物学 Q1 DEVELOPMENTAL BIOLOGY Development Pub Date : 2024-10-15 Epub Date: 2024-10-14 DOI:10.1242/dev.203046
Frédéric Berger
{"title":"减数分裂是表观遗传学重编程和细胞年轻化的一种机制。","authors":"Frédéric Berger","doi":"10.1242/dev.203046","DOIUrl":null,"url":null,"abstract":"<p><p>Meiosis is a hallmark of sexual reproduction because it represents the transition from one life cycle to the next and, in animals, meiosis produces gametes. Why meiosis evolved has been debated and most studies have focused on recombination of the parental alleles as the main function of meiosis. However, 40 years ago, Robin Holliday proposed that an essential function of meiosis is to oppose the consequence of successive mitoses that cause cellular aging. Cellular aging results from accumulated defective organelles and proteins and modifications of chromatin in the form of DNA methylation and histone modifications referred to collectively as epigenetic marks. Here, recent findings supporting the hypothesis that meiosis opposes cellular aging are reviewed and placed in the context of the diversity of the life cycles of eukaryotes, including animals, yeast, flowering plants and the bryophyte Marchantia.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":null,"pages":null},"PeriodicalIF":3.7000,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Meiosis as a mechanism for epigenetic reprogramming and cellular rejuvenation.\",\"authors\":\"Frédéric Berger\",\"doi\":\"10.1242/dev.203046\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Meiosis is a hallmark of sexual reproduction because it represents the transition from one life cycle to the next and, in animals, meiosis produces gametes. Why meiosis evolved has been debated and most studies have focused on recombination of the parental alleles as the main function of meiosis. However, 40 years ago, Robin Holliday proposed that an essential function of meiosis is to oppose the consequence of successive mitoses that cause cellular aging. Cellular aging results from accumulated defective organelles and proteins and modifications of chromatin in the form of DNA methylation and histone modifications referred to collectively as epigenetic marks. Here, recent findings supporting the hypothesis that meiosis opposes cellular aging are reviewed and placed in the context of the diversity of the life cycles of eukaryotes, including animals, yeast, flowering plants and the bryophyte Marchantia.</p>\",\"PeriodicalId\":11375,\"journal\":{\"name\":\"Development\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":3.7000,\"publicationDate\":\"2024-10-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Development\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1242/dev.203046\",\"RegionNum\":2,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/10/14 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"DEVELOPMENTAL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Development","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1242/dev.203046","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/14 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"DEVELOPMENTAL BIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

减数分裂是有性生殖的标志,因为它代表了从一个生命周期到下一个生命周期的过渡,在动物中,减数分裂产生配子。减数分裂为什么会进化一直存在争议,大多数研究都把亲代等位基因的重组作为减数分裂的主要功能。然而,40 年前,罗宾-霍利迪(Robin Holliday)提出,减数分裂的一个基本功能是防止连续有丝分裂导致细胞衰老。细胞衰老的原因是细胞器和蛋白质累积缺陷,以及 DNA 甲基化和组蛋白修饰(统称为表观遗传标记)形式的染色质修饰。本文综述了支持减数分裂抑制细胞衰老这一假说的最新发现,并结合真核生物(包括动物、酵母、开花植物和真叶植物)生命周期的多样性进行了分析。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Meiosis as a mechanism for epigenetic reprogramming and cellular rejuvenation.

Meiosis is a hallmark of sexual reproduction because it represents the transition from one life cycle to the next and, in animals, meiosis produces gametes. Why meiosis evolved has been debated and most studies have focused on recombination of the parental alleles as the main function of meiosis. However, 40 years ago, Robin Holliday proposed that an essential function of meiosis is to oppose the consequence of successive mitoses that cause cellular aging. Cellular aging results from accumulated defective organelles and proteins and modifications of chromatin in the form of DNA methylation and histone modifications referred to collectively as epigenetic marks. Here, recent findings supporting the hypothesis that meiosis opposes cellular aging are reviewed and placed in the context of the diversity of the life cycles of eukaryotes, including animals, yeast, flowering plants and the bryophyte Marchantia.

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
Development
Development 生物-发育生物学
CiteScore
6.70
自引率
4.30%
发文量
433
审稿时长
3 months
期刊介绍: Development’s scope covers all aspects of plant and animal development, including stem cell biology and regeneration. The single most important criterion for acceptance in Development is scientific excellence. Research papers (articles and reports) should therefore pose and test a significant hypothesis or address a significant question, and should provide novel perspectives that advance our understanding of development. We also encourage submission of papers that use computational methods or mathematical models to obtain significant new insights into developmental biology topics. Manuscripts that are descriptive in nature will be considered only when they lay important groundwork for a field and/or provide novel resources for understanding developmental processes of broad interest to the community. Development includes a Techniques and Resources section for the publication of new methods, datasets, and other types of resources. Papers describing new techniques should include a proof-of-principle demonstration that the technique is valuable to the developmental biology community; they need not include in-depth follow-up analysis. The technique must be described in sufficient detail to be easily replicated by other investigators. Development will also consider protocol-type papers of exceptional interest to the community. We welcome submission of Resource papers, for example those reporting new databases, systems-level datasets, or genetic resources of major value to the developmental biology community. For all papers, the data or resource described must be made available to the community with minimal restrictions upon publication. To aid navigability, Development has dedicated sections of the journal to stem cells & regeneration and to human development. The criteria for acceptance into these sections is identical to those outlined above. Authors and editors are encouraged to nominate appropriate manuscripts for inclusion in one of these sections.
期刊最新文献
Differential vegfc expression dictates lymphatic response during zebrafish heart development and regeneration. Establishment of CRISPR/Cas9-based knock-in in a hemimetabolous insect: targeted gene tagging in the cricket Gryllus bimaculatus. The unique functions of Runx1 in skeletal muscle maintenance and regeneration are facilitated by an ETS interaction domain. Contributions of the Dachsous intracellular domain to Dachsous-Fat signaling. Lgr5+ intestinal stem cells are required for organoid survival after genotoxic injury.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1