对 Sae2 C 端在激活 MRX 内切酶中的作用的功能和分子见解。

IF 16.6 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Nucleic Acids Research Pub Date : 2024-11-18 DOI:10.1093/nar/gkae1049
Chiara Vittoria Colombo, Erika Casari, Marco Gnugnoli, Flavio Corallo, Renata Tisi, Maria Pia Longhese
{"title":"对 Sae2 C 端在激活 MRX 内切酶中的作用的功能和分子见解。","authors":"Chiara Vittoria Colombo, Erika Casari, Marco Gnugnoli, Flavio Corallo, Renata Tisi, Maria Pia Longhese","doi":"10.1093/nar/gkae1049","DOIUrl":null,"url":null,"abstract":"<p><p>The yeast Sae2 protein, known as CtIP in mammals, once phosphorylated at Ser267, stimulates the endonuclease activity of the Mre11-Rad50-Xrs2 (MRX) complex to cleave DNA ends that possess hairpin structures or protein blocks, such as the Spo11 transesterase or trapped topoisomerases. Stimulation of the Mre11 endonuclease by Sae2 depends on a Rad50-Sae2 interaction, but the mechanism by which this is achieved remains to be elucidated. Through genetic studies, we show that the absence of the last 23 amino acids from the Sae2 C-terminus specifically impairs MRX-dependent DNA cleavage events, while preserving the other Sae2 functions. Employing AlphaFold3 protein structure predictions, we found that the Rad50-Sae2 interface involves not only phosphorylated Ser267 but also the phosphorylated Thr279 residue and the C-terminus of Sae2. This region engages in multiple interactions with residues that are mutated in rad50-s mutants, which are known to be specifically defective in the processing of Spo11-bound DNA ends. These interactions are critical for stabilizing the association between Sae2 and Rad50, thereby ensuring the correct positioning of Mre11 in its active endonucleolytic state.</p>","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":" ","pages":""},"PeriodicalIF":16.6000,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Functional and molecular insights into the role of Sae2 C-terminus in the activation of MRX endonuclease.\",\"authors\":\"Chiara Vittoria Colombo, Erika Casari, Marco Gnugnoli, Flavio Corallo, Renata Tisi, Maria Pia Longhese\",\"doi\":\"10.1093/nar/gkae1049\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The yeast Sae2 protein, known as CtIP in mammals, once phosphorylated at Ser267, stimulates the endonuclease activity of the Mre11-Rad50-Xrs2 (MRX) complex to cleave DNA ends that possess hairpin structures or protein blocks, such as the Spo11 transesterase or trapped topoisomerases. Stimulation of the Mre11 endonuclease by Sae2 depends on a Rad50-Sae2 interaction, but the mechanism by which this is achieved remains to be elucidated. Through genetic studies, we show that the absence of the last 23 amino acids from the Sae2 C-terminus specifically impairs MRX-dependent DNA cleavage events, while preserving the other Sae2 functions. Employing AlphaFold3 protein structure predictions, we found that the Rad50-Sae2 interface involves not only phosphorylated Ser267 but also the phosphorylated Thr279 residue and the C-terminus of Sae2. This region engages in multiple interactions with residues that are mutated in rad50-s mutants, which are known to be specifically defective in the processing of Spo11-bound DNA ends. These interactions are critical for stabilizing the association between Sae2 and Rad50, thereby ensuring the correct positioning of Mre11 in its active endonucleolytic state.</p>\",\"PeriodicalId\":19471,\"journal\":{\"name\":\"Nucleic Acids Research\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":16.6000,\"publicationDate\":\"2024-11-18\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nucleic Acids Research\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1093/nar/gkae1049\",\"RegionNum\":2,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nucleic Acids Research","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1093/nar/gkae1049","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

酵母 Sae2 蛋白(在哺乳动物中称为 CtIP)一旦在 Ser267 处磷酸化,就会刺激 Mre11-Rad50-Xrs2 (MRX)复合物的内切酶活性,从而裂解具有发夹结构或蛋白块(如 Spo11 转酯酶或被困的拓扑异构酶)的 DNA 末端。Sae2对Mre11内切酶的刺激依赖于Rad50-Sae2的相互作用,但这种作用的机制仍有待阐明。通过基因研究,我们发现 Sae2 C 端最后 23 个氨基酸的缺失会特异性地损害 MRX 依赖性 DNA 裂解事件,同时保留 Sae2 的其他功能。利用 AlphaFold3 蛋白结构预测,我们发现 Rad50-Sae2 界面不仅涉及磷酸化的 Ser267,还涉及磷酸化的 Thr279 残基和 Sae2 的 C-端。该区域与在 rad50-s 突变体中发生突变的残基发生了多种相互作用,众所周知,这些突变体在处理 Spo11 结合的 DNA 末端时存在特异性缺陷。这些相互作用对于稳定 Sae2 和 Rad50 之间的结合至关重要,从而确保 Mre11 在其活性核酸内切状态下的正确定位。
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
Functional and molecular insights into the role of Sae2 C-terminus in the activation of MRX endonuclease.

The yeast Sae2 protein, known as CtIP in mammals, once phosphorylated at Ser267, stimulates the endonuclease activity of the Mre11-Rad50-Xrs2 (MRX) complex to cleave DNA ends that possess hairpin structures or protein blocks, such as the Spo11 transesterase or trapped topoisomerases. Stimulation of the Mre11 endonuclease by Sae2 depends on a Rad50-Sae2 interaction, but the mechanism by which this is achieved remains to be elucidated. Through genetic studies, we show that the absence of the last 23 amino acids from the Sae2 C-terminus specifically impairs MRX-dependent DNA cleavage events, while preserving the other Sae2 functions. Employing AlphaFold3 protein structure predictions, we found that the Rad50-Sae2 interface involves not only phosphorylated Ser267 but also the phosphorylated Thr279 residue and the C-terminus of Sae2. This region engages in multiple interactions with residues that are mutated in rad50-s mutants, which are known to be specifically defective in the processing of Spo11-bound DNA ends. These interactions are critical for stabilizing the association between Sae2 and Rad50, thereby ensuring the correct positioning of Mre11 in its active endonucleolytic state.

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
Nucleic Acids Research
Nucleic Acids Research 生物-生化与分子生物学
CiteScore
27.10
自引率
4.70%
发文量
1057
审稿时长
2 months
期刊介绍: Nucleic Acids Research (NAR) is a scientific journal that publishes research on various aspects of nucleic acids and proteins involved in nucleic acid metabolism and interactions. It covers areas such as chemistry and synthetic biology, computational biology, gene regulation, chromatin and epigenetics, genome integrity, repair and replication, genomics, molecular biology, nucleic acid enzymes, RNA, and structural biology. The journal also includes a Survey and Summary section for brief reviews. Additionally, each year, the first issue is dedicated to biological databases, and an issue in July focuses on web-based software resources for the biological community. Nucleic Acids Research is indexed by several services including Abstracts on Hygiene and Communicable Diseases, Animal Breeding Abstracts, Agricultural Engineering Abstracts, Agbiotech News and Information, BIOSIS Previews, CAB Abstracts, and EMBASE.
期刊最新文献
ClinVar: updates to support classifications of both germline and somatic variants miRStart 2.0: enhancing miRNA regulatory insights through deep learning-based TSS identification miRTarBase 2025: updates to the collection of experimentally validated microRNA-target interactions. GoFCards: an integrated database and analytic platform for gain of function variants in humans. The PIWI-interacting protein Gtsf1 controls the selective degradation of small RNAs in Paramecium
×
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