Xiaoqing Wu , Xin Ming , Qing Liu , Ruisong Bai , Xiaoyu Zhang , Yuheng Bi , Qing Ding , Shangrong Zhang , Jian Li , Hongcheng Wang , Yong Liu
{"title":"敲低Mageb16会破坏小鼠着床前发育过程中的细胞增殖和谱系规范。","authors":"Xiaoqing Wu , Xin Ming , Qing Liu , Ruisong Bai , Xiaoyu Zhang , Yuheng Bi , Qing Ding , Shangrong Zhang , Jian Li , Hongcheng Wang , Yong Liu","doi":"10.1016/j.theriogenology.2025.117391","DOIUrl":null,"url":null,"abstract":"<div><div>Melanoma antigen family member B16 (<em>Mageb16</em>) is crucial for maintaining the pluripotency and differentiation of embryonic stem cells. However, the expression pattern and biological role of <em>Mageb16</em> during preimplantation development remain unclear. In this study, we showed that <em>Mageb1</em>6 mRNA expression was dynamic throughout preimplantation development, with the highest level occurring at the morula stage. The abundance of <em>Mageb1</em>6 mRNA was effectively reduced via small interfering RNA (siRNA) microinjection. <em>Mageb16</em> knockdown significantly reduced the blastocyst formation rate, outgrowth formation rate, and total number of cells per embryo. Importantly, the reduction in MAGEB16 blocked cell cycle progression at the G2/M phase and disrupted lineage segregation but did not induce DNA damage in preimplantation mouse embryos. Intriguingly, <em>Mageb16</em> knockdown increased the level of histone H3 lysine 27 acetylation (H3K27ac) but attenuated transcriptional activity. Together, our results reveal a crucial role for <em>Mageb16</em> in mouse preimplantation development, likely by controlling cell proliferation and lineage specification.</div></div>","PeriodicalId":23131,"journal":{"name":"Theriogenology","volume":"239 ","pages":"Article 117391"},"PeriodicalIF":2.4000,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Knockdown of Mageb16 disrupts cell proliferation and lineage specification during mouse preimplantation development\",\"authors\":\"Xiaoqing Wu , Xin Ming , Qing Liu , Ruisong Bai , Xiaoyu Zhang , Yuheng Bi , Qing Ding , Shangrong Zhang , Jian Li , Hongcheng Wang , Yong Liu\",\"doi\":\"10.1016/j.theriogenology.2025.117391\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Melanoma antigen family member B16 (<em>Mageb16</em>) is crucial for maintaining the pluripotency and differentiation of embryonic stem cells. However, the expression pattern and biological role of <em>Mageb16</em> during preimplantation development remain unclear. In this study, we showed that <em>Mageb1</em>6 mRNA expression was dynamic throughout preimplantation development, with the highest level occurring at the morula stage. The abundance of <em>Mageb1</em>6 mRNA was effectively reduced via small interfering RNA (siRNA) microinjection. <em>Mageb16</em> knockdown significantly reduced the blastocyst formation rate, outgrowth formation rate, and total number of cells per embryo. Importantly, the reduction in MAGEB16 blocked cell cycle progression at the G2/M phase and disrupted lineage segregation but did not induce DNA damage in preimplantation mouse embryos. Intriguingly, <em>Mageb16</em> knockdown increased the level of histone H3 lysine 27 acetylation (H3K27ac) but attenuated transcriptional activity. Together, our results reveal a crucial role for <em>Mageb16</em> in mouse preimplantation development, likely by controlling cell proliferation and lineage specification.</div></div>\",\"PeriodicalId\":23131,\"journal\":{\"name\":\"Theriogenology\",\"volume\":\"239 \",\"pages\":\"Article 117391\"},\"PeriodicalIF\":2.4000,\"publicationDate\":\"2025-03-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Theriogenology\",\"FirstCategoryId\":\"97\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0093691X25001177\",\"RegionNum\":2,\"RegionCategory\":\"农林科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"REPRODUCTIVE BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Theriogenology","FirstCategoryId":"97","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0093691X25001177","RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"REPRODUCTIVE BIOLOGY","Score":null,"Total":0}
Knockdown of Mageb16 disrupts cell proliferation and lineage specification during mouse preimplantation development
Melanoma antigen family member B16 (Mageb16) is crucial for maintaining the pluripotency and differentiation of embryonic stem cells. However, the expression pattern and biological role of Mageb16 during preimplantation development remain unclear. In this study, we showed that Mageb16 mRNA expression was dynamic throughout preimplantation development, with the highest level occurring at the morula stage. The abundance of Mageb16 mRNA was effectively reduced via small interfering RNA (siRNA) microinjection. Mageb16 knockdown significantly reduced the blastocyst formation rate, outgrowth formation rate, and total number of cells per embryo. Importantly, the reduction in MAGEB16 blocked cell cycle progression at the G2/M phase and disrupted lineage segregation but did not induce DNA damage in preimplantation mouse embryos. Intriguingly, Mageb16 knockdown increased the level of histone H3 lysine 27 acetylation (H3K27ac) but attenuated transcriptional activity. Together, our results reveal a crucial role for Mageb16 in mouse preimplantation development, likely by controlling cell proliferation and lineage specification.
期刊介绍:
Theriogenology provides an international forum for researchers, clinicians, and industry professionals in animal reproductive biology. This acclaimed journal publishes articles on a wide range of topics in reproductive and developmental biology, of domestic mammal, avian, and aquatic species as well as wild species which are the object of veterinary care in research or conservation programs.