{"title":"男性特异性保守LncRNA TSCL1通过与PIWIL1相互作用调控靶mRNA翻译。","authors":"Shuai Lu, Yang Li, Chenmeijie Li, Zhongyu Zou, Xiaoxi Xu, Shijie Zhu, Beibei Yang, Gaoming Tang, Haoran Chen, Yuchen Wang, Feng Li, Na Qin, Cheng Wang, Hongbing Shen, Zhibin Hu, Yayun Gu","doi":"10.1038/s41418-025-01583-8","DOIUrl":null,"url":null,"abstract":"<p><p>Long non-coding RNAs (lncRNAs) play crucial roles in diverse mammalian physiological processes, yet their functions in spermatogenesis remain largely underexplored. Here, we identify a unique class of conserved haploid spermatid-associated lncRNAs (cHS-LncRNAs) defined by sequence conservation, testis-restricted expression, and elevated levels in haploid spermatids. Among these, testis-specific conserved lncRNA 1 (Tscl1) is the most highly expressed in round spermatids. Tscl1-null male mice exhibit reduced sperm motility, disorganized mitochondrial sheaths, abnormal fatty acid metabolism, and complete infertility. Mechanistically, Tscl1 directly binds PIWIL1 and HuR via its 5' stem-loop and multiple AU-rich elements, respectively. This interaction promotes assembly of a PIWIL1/eIF3f/HuR/eIF4G3 complex that enhances translation of fatty-acid-metabolism-related mRNAs within the chromatoid body. Notably, TSCL1 variants disrupting the PIWIL1-binding region are significantly enriched in patients with non-obstructive azoospermia (NOA) compared to fertile controls. Collectively, our findings uncover a critical role for Tscl1 in modulating translation during spermiogenesis and implicate TSCL1 as a potential pathogenic locus in human male infertility.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":" ","pages":""},"PeriodicalIF":15.4000,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Male specific conserved LncRNA TSCL1 regulated target mRNA translation by interaction with PIWIL1.\",\"authors\":\"Shuai Lu, Yang Li, Chenmeijie Li, Zhongyu Zou, Xiaoxi Xu, Shijie Zhu, Beibei Yang, Gaoming Tang, Haoran Chen, Yuchen Wang, Feng Li, Na Qin, Cheng Wang, Hongbing Shen, Zhibin Hu, Yayun Gu\",\"doi\":\"10.1038/s41418-025-01583-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Long non-coding RNAs (lncRNAs) play crucial roles in diverse mammalian physiological processes, yet their functions in spermatogenesis remain largely underexplored. Here, we identify a unique class of conserved haploid spermatid-associated lncRNAs (cHS-LncRNAs) defined by sequence conservation, testis-restricted expression, and elevated levels in haploid spermatids. Among these, testis-specific conserved lncRNA 1 (Tscl1) is the most highly expressed in round spermatids. Tscl1-null male mice exhibit reduced sperm motility, disorganized mitochondrial sheaths, abnormal fatty acid metabolism, and complete infertility. Mechanistically, Tscl1 directly binds PIWIL1 and HuR via its 5' stem-loop and multiple AU-rich elements, respectively. This interaction promotes assembly of a PIWIL1/eIF3f/HuR/eIF4G3 complex that enhances translation of fatty-acid-metabolism-related mRNAs within the chromatoid body. Notably, TSCL1 variants disrupting the PIWIL1-binding region are significantly enriched in patients with non-obstructive azoospermia (NOA) compared to fertile controls. Collectively, our findings uncover a critical role for Tscl1 in modulating translation during spermiogenesis and implicate TSCL1 as a potential pathogenic locus in human male infertility.</p>\",\"PeriodicalId\":9731,\"journal\":{\"name\":\"Cell Death and Differentiation\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":15.4000,\"publicationDate\":\"2025-09-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cell Death and Differentiation\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1038/s41418-025-01583-8\",\"RegionNum\":1,\"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":"Cell Death and Differentiation","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1038/s41418-025-01583-8","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Male specific conserved LncRNA TSCL1 regulated target mRNA translation by interaction with PIWIL1.
Long non-coding RNAs (lncRNAs) play crucial roles in diverse mammalian physiological processes, yet their functions in spermatogenesis remain largely underexplored. Here, we identify a unique class of conserved haploid spermatid-associated lncRNAs (cHS-LncRNAs) defined by sequence conservation, testis-restricted expression, and elevated levels in haploid spermatids. Among these, testis-specific conserved lncRNA 1 (Tscl1) is the most highly expressed in round spermatids. Tscl1-null male mice exhibit reduced sperm motility, disorganized mitochondrial sheaths, abnormal fatty acid metabolism, and complete infertility. Mechanistically, Tscl1 directly binds PIWIL1 and HuR via its 5' stem-loop and multiple AU-rich elements, respectively. This interaction promotes assembly of a PIWIL1/eIF3f/HuR/eIF4G3 complex that enhances translation of fatty-acid-metabolism-related mRNAs within the chromatoid body. Notably, TSCL1 variants disrupting the PIWIL1-binding region are significantly enriched in patients with non-obstructive azoospermia (NOA) compared to fertile controls. Collectively, our findings uncover a critical role for Tscl1 in modulating translation during spermiogenesis and implicate TSCL1 as a potential pathogenic locus in human male infertility.
期刊介绍:
Mission, vision and values of Cell Death & Differentiation:
To devote itself to scientific excellence in the field of cell biology, molecular biology, and biochemistry of cell death and disease.
To provide a unified forum for scientists and clinical researchers
It is committed to the rapid publication of high quality original papers relating to these subjects, together with topical, usually solicited, reviews, meeting reports, editorial correspondence and occasional commentaries on controversial and scientifically informative issues.