Germline loss in C. elegans enhances longevity by disrupting adhesion between niche and stem cells.

IF 9.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
EMBO Journal Pub Date : 2024-09-01 Epub Date: 2024-07-25 DOI:10.1038/s44318-024-00185-3
Meng Liu, Jiehui Chen, Guizhong Cui, Yumin Dai, Mengjiao Song, Chunyu Zhou, Qingyuan Hu, Qingxia Chen, Hongwei Wang, Wanli Chen, Jingdong Jackie Han, Guangdun Peng, Naihe Jing, Yidong Shen
{"title":"Germline loss in C. elegans enhances longevity by disrupting adhesion between niche and stem cells.","authors":"Meng Liu, Jiehui Chen, Guizhong Cui, Yumin Dai, Mengjiao Song, Chunyu Zhou, Qingyuan Hu, Qingxia Chen, Hongwei Wang, Wanli Chen, Jingdong Jackie Han, Guangdun Peng, Naihe Jing, Yidong Shen","doi":"10.1038/s44318-024-00185-3","DOIUrl":null,"url":null,"abstract":"<p><p>Ageing and fertility are intertwined. Germline loss extends the lifespan in various organisms, termed gonadal longevity. However, the original longevity signal from the somatic gonad remains poorly understood. Here, we focused on the interaction between germline stem cells (GSCs) and their niche, the distal tip cells (DTCs), to explore the barely known longevity signal from the somatic gonad in C. elegans. We found that removing germline disrupts the cell adhesions between GSC and DTC, causing a significant transcriptomic change in DTC through hmp-2/β-catenin and two GATA transcription factors, elt-3 and pqm-1 in this niche cell. Inhibiting elt-3 and pqm-1 in DTC suppresses gonadal longevity. Moreover, we further identified the TGF-β ligand, tig-2, as the cytokine from DTC upon the loss of germline, which evokes the downstream gonadal longevity signalling throughout the body. Our findings thus reveal the source of the longevity signalling in response to germline removal, highlighting the stem cell niche as a critical signalling hub in ageing.</p>","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":"4000-4019"},"PeriodicalIF":9.4000,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11405865/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"EMBO Journal","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1038/s44318-024-00185-3","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/7/25 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Ageing and fertility are intertwined. Germline loss extends the lifespan in various organisms, termed gonadal longevity. However, the original longevity signal from the somatic gonad remains poorly understood. Here, we focused on the interaction between germline stem cells (GSCs) and their niche, the distal tip cells (DTCs), to explore the barely known longevity signal from the somatic gonad in C. elegans. We found that removing germline disrupts the cell adhesions between GSC and DTC, causing a significant transcriptomic change in DTC through hmp-2/β-catenin and two GATA transcription factors, elt-3 and pqm-1 in this niche cell. Inhibiting elt-3 and pqm-1 in DTC suppresses gonadal longevity. Moreover, we further identified the TGF-β ligand, tig-2, as the cytokine from DTC upon the loss of germline, which evokes the downstream gonadal longevity signalling throughout the body. Our findings thus reveal the source of the longevity signalling in response to germline removal, highlighting the stem cell niche as a critical signalling hub in ageing.

秀丽隐杆线虫的种系缺失会破坏龛位细胞和干细胞之间的粘附,从而延长寿命。
衰老和生育能力是相互交织的。生殖细胞的丧失延长了各种生物的寿命,这就是所谓的性腺长寿。然而,人们对来自体细胞性腺的原始长寿信号仍然知之甚少。在这里,我们重点研究了生殖干细胞(GSCs)与其生态位--远端顶端细胞(DTCs)--之间的相互作用,以探索 elegans 中几乎不为人知的来自体细胞性腺的长寿信号。我们发现,移除生殖细胞会破坏GSC和DTC之间的细胞粘附,并通过hmp-2/β-catenin和两个GATA转录因子elt-3和pqm-1导致DTC的转录组发生显著变化。抑制DTC中的elt-3和pqm-1可抑制性腺寿命。此外,我们还进一步确定了 TGF-β 配体 tig-2 是 DTC 在失去生殖细胞后产生的细胞因子,它唤起了整个身体的下游性腺长寿信号。因此,我们的研究结果揭示了生殖细胞被切除后长寿信号的来源,凸显了干细胞龛是衰老过程中一个关键的信号枢纽。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
EMBO Journal
EMBO Journal 生物-生化与分子生物学
CiteScore
18.90
自引率
0.90%
发文量
246
审稿时长
1.5 months
期刊介绍: The EMBO Journal has stood as EMBO's flagship publication since its inception in 1982. Renowned for its international reputation in quality and originality, the journal spans all facets of molecular biology. It serves as a platform for papers elucidating original research of broad general interest in molecular and cell biology, with a distinct focus on molecular mechanisms and physiological relevance. With a commitment to promoting articles reporting novel findings of broad biological significance, The EMBO Journal stands as a key contributor to advancing the field of molecular biology.
×
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:481959085
Book学术官方微信