父亲的饮食定义了后代的染色质状况和代际肥胖症
Anita Öst1, Adelheid Lempradl2, Eduard Casas3
1Max Planck Institute of Immunobiology and Epigenetics, Stuebeweg 51, 79108 Freiburg, Germany; Department of Clinical and Experimental Medicine, Linkoping University, 58183 Linkoping, Sweden.
Cell
|December 7, 2014
概括
父亲摄入的糖可以通过代际代谢重编程 (IGMR) 导致后代肥胖. 这通过精子的表观遗传变化发生,影响后代.
科学领域:
- 遗传学和表观遗传学
- 发展生物学 发展生物学
- 代谢疾病研究研究
背景情况:
- 全球肥胖率的上升需要了解遗传和表观遗传因素.
- 代际代谢重编程 (IGMR) 是一个关键的研究领域.
- 人们越来越认识到,父亲的饮食对后代健康的影响.
研究的目的:
- 为了建立一个Drosophila模型,用于父饮食诱导的IGMR.
- 在后代中识别参与编码IGMR的基因.
- 研究将父亲饮食与后代肥胖症联系在一起的表观遗传机制.
主要方法:
- 使用了一种Drosophila melanogaster模型系统.
- 进行了短期的父亲饮食干预 (糖).
- 分析精子和后代胚胎表观遗传学 (H3K9/K27me3) 和基因表达.
主要成果:
- 只有2天的父亲糖饮食导致后代肥胖.
- 父亲糖作为一个生理抑制器的变异, desilencing 染色质域在精子和胚胎.
- 鉴定了H3K9/K27me3-依赖的代谢基因在生殖和胚胎阶段的重编程.
- 观察到小鼠和人类在肥胖易感性和表型变异方面存在潜在的相似性.
结论:
- 父亲的饮食可以在几代人之间以表观遗传方式重新编程后代的新陈代谢.
- 对于IGMR来说,特定的组素修饰 (H3K9/K27me3) 是至关重要的.
- 这些发现表明,物种之间存在IGMR的保存机制,影响进化和表型变异.
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