The role of Smarcad1 in retroviral repression in mouse embryonic stem cells

IF 4.7 2区 生物学 Q1 GENETICS & HEREDITY Mobile DNA Pub Date : 2024-03-11 DOI:10.1186/s13100-024-00314-z
Igor Bren, Ayellet Tal, Carmit Strauss, Sharon Schlesinger
{"title":"The role of Smarcad1 in retroviral repression in mouse embryonic stem cells","authors":"Igor Bren, Ayellet Tal, Carmit Strauss, Sharon Schlesinger","doi":"10.1186/s13100-024-00314-z","DOIUrl":null,"url":null,"abstract":"Moloney murine leukemia virus (MLV) replication is suppressed in mouse embryonic stem cells (ESCs) by the Trim28-SETDB1 complex. The chromatin remodeler Smarcad1 interacts with Trim28 and was suggested to allow the deposition of the histone variant H3.3. However, the role of Trim28, H3.3, and Smarcad1 in MLV repression in ESCs still needs to be fully understood. In this study, we used MLV to explore the role of Smarcad1 in retroviral silencing in ESCs. We show that Smarcad1 is immediately recruited to the MLV provirus. Based on the repression dynamics of a GFP-reporter MLV, our findings suggest that Smarcad1 plays a critical role in the establishment and maintenance of MLV repression, as well as other Trim28-targeted genomic loci. Furthermore, Smarcad1 is important for stabilizing and strengthening Trim28 binding to the provirus over time, and its presence around the provirus is needed for proper deposition of H3.3 on the provirus. Surprisingly, the combined depletion of Smarcad1 and Trim28 results in enhanced MLV derepression, suggesting that these two proteins may also function independently to maintain repressive chromatin states. Overall, the results of this study provide evidence for the crucial role of Smarcad1 in the silencing of retroviral elements in embryonic stem cells. Further research is needed to fully understand how Smarcad1 and Trim28 cooperate and their implications for gene expression and genomic stability.","PeriodicalId":18854,"journal":{"name":"Mobile DNA","volume":"90 1","pages":""},"PeriodicalIF":4.7000,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mobile DNA","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s13100-024-00314-z","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
引用次数: 0

Abstract

Moloney murine leukemia virus (MLV) replication is suppressed in mouse embryonic stem cells (ESCs) by the Trim28-SETDB1 complex. The chromatin remodeler Smarcad1 interacts with Trim28 and was suggested to allow the deposition of the histone variant H3.3. However, the role of Trim28, H3.3, and Smarcad1 in MLV repression in ESCs still needs to be fully understood. In this study, we used MLV to explore the role of Smarcad1 in retroviral silencing in ESCs. We show that Smarcad1 is immediately recruited to the MLV provirus. Based on the repression dynamics of a GFP-reporter MLV, our findings suggest that Smarcad1 plays a critical role in the establishment and maintenance of MLV repression, as well as other Trim28-targeted genomic loci. Furthermore, Smarcad1 is important for stabilizing and strengthening Trim28 binding to the provirus over time, and its presence around the provirus is needed for proper deposition of H3.3 on the provirus. Surprisingly, the combined depletion of Smarcad1 and Trim28 results in enhanced MLV derepression, suggesting that these two proteins may also function independently to maintain repressive chromatin states. Overall, the results of this study provide evidence for the crucial role of Smarcad1 in the silencing of retroviral elements in embryonic stem cells. Further research is needed to fully understand how Smarcad1 and Trim28 cooperate and their implications for gene expression and genomic stability.
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
Smarcad1 在小鼠胚胎干细胞逆转录病毒抑制中的作用
小鼠胚胎干细胞(ESC)中的莫洛尼小鼠白血病病毒(MLV)复制受到Trim28-SETDB1复合物的抑制。染色质重塑者Smarcad1与Trim28相互作用,并被认为允许组蛋白变体H3.3的沉积。然而,Trim28、H3.3和Smarcad1在MLV抑制ESC中的作用仍有待全面了解。在这项研究中,我们利用MLV来探讨Smarcad1在ESC中逆转录病毒沉默中的作用。我们发现Smarcad1会被立即招募到MLV病毒上。基于GFP报告的MLV的抑制动态,我们的研究结果表明,Smarcad1在MLV抑制以及其他Trim28靶向基因组位点的建立和维持中起着关键作用。此外,随着时间的推移,Smarcad1 对稳定和加强 Trim28 与前病毒的结合非常重要,前病毒周围需要有 Smarcad1 才能使 H3.3 适当地沉积在前病毒上。令人惊讶的是,联合消耗 Smarcad1 和 Trim28 会增强 MLV 的抑制作用,这表明这两种蛋白也可能独立发挥作用,维持抑制性染色质状态。总之,本研究结果为Smarcad1在胚胎干细胞中沉默逆转录病毒元件的关键作用提供了证据。要全面了解Smarcad1和Trim28如何合作及其对基因表达和基因组稳定性的影响,还需要进一步的研究。
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 去求助
来源期刊
Mobile DNA
Mobile DNA GENETICS & HEREDITY-
CiteScore
8.20
自引率
6.10%
发文量
26
审稿时长
11 weeks
期刊介绍: Mobile DNA is an online, peer-reviewed, open access journal that publishes articles providing novel insights into DNA rearrangements in all organisms, ranging from transposition and other types of recombination mechanisms to patterns and processes of mobile element and host genome evolution. In addition, the journal will consider articles on the utility of mobile genetic elements in biotechnological methods and protocols.
期刊最新文献
Analysis of pericentromere composition and structure elucidated the history of the Hieracium alpinum L. genome, revealing waves of transposable elements insertions. International congress on transposable elements (ICTE 2024) in Saint Malo: breaking down transposon waves and their impact. Accelerating de novo SINE annotation in plant and animal genomes. Association of hyperactivated transposon expression with exacerbated immune activation in systemic lupus erythematosus. Widespread HCD-tRNA derived SINEs in bivalves rely on multiple LINE partners and accumulate in genic regions.
×
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