The maize mTERF18 regulates transcriptional termination of the mitochondrial nad6 gene and is essential for kernel development.

IF 6.6 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Genetics and Genomics Pub Date : 2025-01-09 DOI:10.1016/j.jgg.2025.01.001
Zhengwei Guan, Yong Wang, Jun Yang
{"title":"The maize mTERF18 regulates transcriptional termination of the mitochondrial nad6 gene and is essential for kernel development.","authors":"Zhengwei Guan, Yong Wang, Jun Yang","doi":"10.1016/j.jgg.2025.01.001","DOIUrl":null,"url":null,"abstract":"<p><p>Mitochondria are semi-autonomous organelles present in eukaryotic cells, containing their own genome and transcriptional machinery. However, their functions are intricately linked to proteins encoded by the nuclear genome. Mitochondrial transcription termination factors (mTERFs) are nucleic acid-binding proteins involved in RNA splicing and transcription termination within plant mitochondria and chloroplasts. Despite their recognized importance, the specific roles of mTERF proteins in maize remain largely unexplored. Here, we clone and functionally characterize the maize mTERF18 gene. Our findings reveal that mTERF18 mutations lead to severely undifferentiated embryos, resulting in abortive phenotypes. Early kernel exhibits abnormal basal endosperm transfer layer and a significant reduction in both starch and protein accumulation in mterf18. We identify the mTERF18 gene through mapping-based cloning and validate this gene through allelic tests. mTERF18 is widely expressed across various maize tissues and encodes a highly conserved mitochondrial protein. Transcriptome data reveal that mTERF18 mutations disrupt transcriptional termination of the nad6 gene, leading to undetectable levels of Nad6 protein and reduced complex I assembly and activity. Furthermore, transmission electron microscopy observation of mterf18 endosperm uncover severe mitochondrial defects. Collectively, these findings highlight the critical role of mTERF18 in mitochondrial gene transcription termination and its pivotal impact on maize kernel development.</p>","PeriodicalId":54825,"journal":{"name":"Journal of Genetics and Genomics","volume":" ","pages":""},"PeriodicalIF":6.6000,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Genetics and Genomics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/j.jgg.2025.01.001","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

Abstract

Mitochondria are semi-autonomous organelles present in eukaryotic cells, containing their own genome and transcriptional machinery. However, their functions are intricately linked to proteins encoded by the nuclear genome. Mitochondrial transcription termination factors (mTERFs) are nucleic acid-binding proteins involved in RNA splicing and transcription termination within plant mitochondria and chloroplasts. Despite their recognized importance, the specific roles of mTERF proteins in maize remain largely unexplored. Here, we clone and functionally characterize the maize mTERF18 gene. Our findings reveal that mTERF18 mutations lead to severely undifferentiated embryos, resulting in abortive phenotypes. Early kernel exhibits abnormal basal endosperm transfer layer and a significant reduction in both starch and protein accumulation in mterf18. We identify the mTERF18 gene through mapping-based cloning and validate this gene through allelic tests. mTERF18 is widely expressed across various maize tissues and encodes a highly conserved mitochondrial protein. Transcriptome data reveal that mTERF18 mutations disrupt transcriptional termination of the nad6 gene, leading to undetectable levels of Nad6 protein and reduced complex I assembly and activity. Furthermore, transmission electron microscopy observation of mterf18 endosperm uncover severe mitochondrial defects. Collectively, these findings highlight the critical role of mTERF18 in mitochondrial gene transcription termination and its pivotal impact on maize kernel development.

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
玉米mTERF18调控线粒体nad6基因的转录终止,对玉米籽粒发育至关重要。
线粒体是存在于真核细胞中的半自主细胞器,包含自己的基因组和转录机制。然而,它们的功能与核基因组编码的蛋白质有着复杂的联系。线粒体转录终止因子(mTERFs)是植物线粒体和叶绿体中参与RNA剪接和转录终止的核酸结合蛋白。尽管它们具有公认的重要性,但mTERF蛋白在玉米中的具体作用在很大程度上仍未被探索。本文对玉米mTERF18基因进行了克隆和功能表征。我们的研究结果表明,mTERF18突变导致胚胎严重未分化,导致表型流产。mterf18在籽粒早期表现出基乳转移层异常,淀粉和蛋白质积累显著减少。我们通过定位克隆鉴定了mTERF18基因,并通过等位基因测试对该基因进行了验证。mTERF18在多种玉米组织中广泛表达,编码一种高度保守的线粒体蛋白。转录组数据显示,mTERF18突变破坏了nad6基因的转录终止,导致nad6蛋白水平无法检测,复合物I的组装和活性降低。此外,透射电镜观察mterf18胚乳发现严重的线粒体缺陷。总之,这些发现突出了mTERF18在线粒体基因转录终止中的关键作用及其对玉米籽粒发育的关键影响。
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
Journal of Genetics and Genomics
Journal of Genetics and Genomics 生物-生化与分子生物学
CiteScore
8.20
自引率
3.40%
发文量
4756
审稿时长
14 days
期刊介绍: The Journal of Genetics and Genomics (JGG, formerly known as Acta Genetica Sinica ) is an international journal publishing peer-reviewed articles of novel and significant discoveries in the fields of genetics and genomics. Topics of particular interest include but are not limited to molecular genetics, developmental genetics, cytogenetics, epigenetics, medical genetics, population and evolutionary genetics, genomics and functional genomics as well as bioinformatics and computational biology.
期刊最新文献
Resolving the spatial and cellular architecture of intra-tumor heterogeneity by multi-region dissection of lung adenocarcinoma. Expression quantitative trait loci (eQTL): from population genetics to precision medicine. A gain-of-function variant in RICTOR predisposes to human obesity. Diverse functions of sex determination gene doublesex on sexually dimorphic neuronal development and behaviors. Unlocking soybean potential: genetic resources and omics for breeding.
×
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