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使用基于内在无序区域(IDR)的策略扩展RNA编辑工具包。

Expanding RNA editing toolkit using an IDR-based strategy.

作者信息

Di Minghui, Lv Junjun, Jing Zhengyu, Yang Yijie, Yan Kunlun, Wu Jianguo, Ge Jianyang, Rauch Simone, Dickinson Bryan C, Chi Tian

机构信息

School of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China.

Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai 200031, China.

出版信息

Mol Ther Nucleic Acids. 2024 Apr 16;35(2):102190. doi: 10.1016/j.omtn.2024.102190. eCollection 2024 Jun 11.

Abstract

RNA base editors should ideally be free of immunogenicity, compact, efficient, and specific, which has not been achieved for C > U editing. Here we first describe a compact C > U editor entirely of human origin, created by fusing the human C > U editing enzyme RESCUE-S to Cas inspired RNA targeting system (CIRTS), a tiny, human-originated programmable RNA-binding domain. This editor, CIRTS-RESCUEv1 (V1), was inefficient. Remarkably, a short histidine-rich domain (HRD), which is derived from the internal disordered region (IDR) in the human CYCT1, a protein capable of liquid-liquid phase separation (LLPS), enhanced V1 editing at on-targets as well as off-targets, the latter effect being minor. The V1-HRD fusion protein formed puncta characteristic of LLPS, and various other IDRs (but not an LLPS-impaired mutant) could replace HRD to effectively induce puncta and potentiate V1, suggesting that the diverse domains acted via a common, LLPS-based mechanism. Importantly, the HRD fusion strategy was applicable to various other types of C > U RNA editors. Our study expands the RNA editing toolbox and showcases a general method for stimulating C > U RNA base editors.

摘要

理想情况下,RNA碱基编辑器应无免疫原性、结构紧凑、高效且具有特异性,而C>U编辑尚未实现这些目标。在此,我们首先描述一种完全源自人类的紧凑型C>U编辑器,它是通过将人类C>U编辑酶RESCUE-S与受Cas启发的RNA靶向系统(CIRTS,一种微小的、源自人类的可编程RNA结合结构域)融合而创建的。这种编辑器,即CIRTS-RESCUEv1(V1),效率不高。值得注意的是,一个源自人类CYCT1内部无序区域(IDR)的富含组氨酸的短结构域(HRD)增强了V1在靶标和脱靶位点的编辑能力,后者的影响较小。V1-HRD融合蛋白形成了液-液相分离(LLPS)特有的斑点,并且各种其他IDR(但不是LLPS受损的突变体)可以替代HRD来有效诱导斑点并增强V1,这表明不同的结构域通过基于LLPS的共同机制发挥作用。重要的是,HRD融合策略适用于各种其他类型的C>U RNA编辑器。我们的研究扩展了RNA编辑工具箱,并展示了一种刺激C>U RNA碱基编辑器的通用方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04c5/11077028/8b1cb485a44c/fx1.jpg

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