{"title":"Dcun1d3在小鼠精子发生和雄性生殖中是不可缺少的。","authors":"Meng Liu, Wenxin Gao, Wenyi Sheng, Nianchao Zhou, Tiantian Wu, Cong Shen, Guannan Feng, Xiaoxue Xi","doi":"10.62347/BZPE6333","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>DCUN1D3, a member of the DCNL (defective in cullin neddylation-like) protein family, has been implicated in ultraviolet (UV) radiation-induced cell cycle checkpoints, cell growth, survival, and neddylation. However, its specific function in male germ cells and potential involvement in spermatogenesis remain poorly understood.</p><p><strong>Methods: </strong>To investigate the role of Dcun1d3 in male reproduction, we generated <i>Dcun1d3</i> knockout (KO) mice. Sperm parameters were evaluated using computer-assisted sperm analysis (CASA), while histological and immunohistochemical analyses were performed to assess spermatogenesis.</p><p><strong>Results: </strong><i>Dcun1d3</i>-KO mice exhibited no significant differences in testicular histology, sperm quality, levels of germ cell apoptosis, or fertility outcomes compared to wild-type controls.</p><p><strong>Conclusions: </strong>These findings indicate that Dcun1d3 is not essential for spermatogenesis or male fertility in mice. This study provides evidence to streamline future investigations by excluding Dcun1d3 as a critical regulator of male germ cell development and offers useful insights for human fertility gene research.</p>","PeriodicalId":72163,"journal":{"name":"American journal of clinical and experimental immunology","volume":"14 3","pages":"127-137"},"PeriodicalIF":1.3000,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12267095/pdf/","citationCount":"0","resultStr":"{\"title\":\"Dcun1d3 is dispensable for spermatogenesis and male fertility in mice.\",\"authors\":\"Meng Liu, Wenxin Gao, Wenyi Sheng, Nianchao Zhou, Tiantian Wu, Cong Shen, Guannan Feng, Xiaoxue Xi\",\"doi\":\"10.62347/BZPE6333\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>DCUN1D3, a member of the DCNL (defective in cullin neddylation-like) protein family, has been implicated in ultraviolet (UV) radiation-induced cell cycle checkpoints, cell growth, survival, and neddylation. However, its specific function in male germ cells and potential involvement in spermatogenesis remain poorly understood.</p><p><strong>Methods: </strong>To investigate the role of Dcun1d3 in male reproduction, we generated <i>Dcun1d3</i> knockout (KO) mice. Sperm parameters were evaluated using computer-assisted sperm analysis (CASA), while histological and immunohistochemical analyses were performed to assess spermatogenesis.</p><p><strong>Results: </strong><i>Dcun1d3</i>-KO mice exhibited no significant differences in testicular histology, sperm quality, levels of germ cell apoptosis, or fertility outcomes compared to wild-type controls.</p><p><strong>Conclusions: </strong>These findings indicate that Dcun1d3 is not essential for spermatogenesis or male fertility in mice. This study provides evidence to streamline future investigations by excluding Dcun1d3 as a critical regulator of male germ cell development and offers useful insights for human fertility gene research.</p>\",\"PeriodicalId\":72163,\"journal\":{\"name\":\"American journal of clinical and experimental immunology\",\"volume\":\"14 3\",\"pages\":\"127-137\"},\"PeriodicalIF\":1.3000,\"publicationDate\":\"2025-06-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12267095/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American journal of clinical and experimental immunology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.62347/BZPE6333\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q4\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American journal of clinical and experimental immunology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.62347/BZPE6333","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q4","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
Dcun1d3 is dispensable for spermatogenesis and male fertility in mice.
Background: DCUN1D3, a member of the DCNL (defective in cullin neddylation-like) protein family, has been implicated in ultraviolet (UV) radiation-induced cell cycle checkpoints, cell growth, survival, and neddylation. However, its specific function in male germ cells and potential involvement in spermatogenesis remain poorly understood.
Methods: To investigate the role of Dcun1d3 in male reproduction, we generated Dcun1d3 knockout (KO) mice. Sperm parameters were evaluated using computer-assisted sperm analysis (CASA), while histological and immunohistochemical analyses were performed to assess spermatogenesis.
Results: Dcun1d3-KO mice exhibited no significant differences in testicular histology, sperm quality, levels of germ cell apoptosis, or fertility outcomes compared to wild-type controls.
Conclusions: These findings indicate that Dcun1d3 is not essential for spermatogenesis or male fertility in mice. This study provides evidence to streamline future investigations by excluding Dcun1d3 as a critical regulator of male germ cell development and offers useful insights for human fertility gene research.
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