美国斯坦福大学Anne Brunet等研究人员合作发现，非洲青鳉鱼通过重塑古老基因调控格局实现滞育演化。2024年5月28日，《细胞》杂志在线发表了这项成果。

为了了解滞育演化，研究人员对多个鳉鱼物种的胚胎进行了综合多组学研究（基因表达、染色质可及性和脂质组学）。研究人员发现，在所有脊椎动物中都存在的非常古老的基因重复序列（旁系同源物）上的调控元件，是通过最近的重塑演化而来的。基于CRISPR-Cas9的扰动发现，转录因子REST/NRSF和FOXO对滞育基因表达程序至关重要，包括参与脂质代谢的基因。

事实上，滞育表现出独特的脂质特征，含有超长链脂肪酸的甘油三酯增加。该研究为复杂适应性的演化提供了一种机制，并为通过激活其他物种的滞育程序来促进长期生存提供了策略。

据了解，休眠状态允许生物体在极端环境中生存。非洲青鳉鱼已经进化出了一种延迟发育的方式，可以在完全干旱的情况下生存。然而，极端生存状态的进化机制尚不清楚。

附：英文原文

Title: Evolution of diapause in the African turquoise killifish by remodeling the ancient gene regulatory landscape

Author: Param Priya Singh, G. Adam Reeves, Kévin Contrepois, Katharina Papsdorf, Jason W. Miklas, Mathew Ellenberger, Chi-Kuo Hu, Michael P. Snyder, Anne Brunet

Issue&Volume: 2024-05-28

Abstract: Suspended animation states allow organisms to survive extreme environments. The African turquoise killifish has evolved diapause as a form of suspended development to survive a complete drought. However, the mechanisms underlying the evolution of extreme survival states are unknown. To understand diapause evolution, we performed integrative multi-omics (gene expression, chromatin accessibility, and lipidomics) in the embryos of multiple killifish species. We find that diapause evolved by a recent remodeling of regulatory elements at very ancient gene duplicates (paralogs) present in all vertebrates. CRISPR-Cas9-based perturbations identify the transcription factors REST/NRSF and FOXOs as critical for the diapause gene expression program, including genes involved in lipid metabolism. Indeed, diapause shows a distinct lipid profile, with an increase in triglycerides with very-long-chain fatty acids. Our work suggests a mechanism for the evolution of complex adaptations and offers strategies to promote long-term survival by activating suspended animation programs in other species.

DOI: 10.1016/j.cell.2024.04.048

Source: https://www.cell.com/cell/fulltext/S0092-8674(24)00474-4

期刊信息

Cell：《细胞》，创刊于1974年。隶属于细胞出版社，最新IF：66.85

官方网址：https://www.cell.com

投稿链接：https://www.editorialmanager.com/cell/default.aspx