哈佛医学院Scott Kennedy小组的一项最新研究开发出了从动物mRNAs中切除DNA转座子的RNA剪接系统。这一研究成果发表在2025年12月10日出版的国际学术期刊《自然》上。

在这里，研究团队描述了一个系统，称之为SOS剪接，保护秀丽隐杆线虫和人类基因免受DNA转座子介导的破坏，通过从宿主mRNAs中切除这些TEs。SOS剪接是一种模式识别系统，它似乎独立于剪接体运作，是由DNA转座子的一个定义特征——反向末端重复元件的碱基配对触发的。秀丽隐杆线虫和人类细胞中鉴定出SOS剪接必需的三个关键因子：AKAP17A，它结合含有TEs的mRNAs；RNA连接酶RTCB；以及连接RTCB和AKAP17A的CAAP1，使RTCB能够连接TE切除产生的mRNA片段。研究小组提出，SOS剪接是一种先前未被描述的保守的RNA结构导向的mRNA剪接模式，并且SOS剪接的一个已确定的功能是在基因上缓冲动物免受DNA转座子介导的基因扰动的有害影响。

研究人员表示，所有基因组都有可移动的基因片段，称为转座因子（TEs）。

附：英文原文

Title: An RNA splicing system that excises DNA transposons from animal mRNAs

Author: Zhao, Long-Wen, Nardone, Christopher, Chang, Cindy, Paulo, Joao A., Elledge, Stephen J., Kennedy, Scott

Issue&Volume: 2025-12-10

Abstract: All genomes have mobile genetic segments called transposable elements (TEs)1. Here we describe a system, which we term SOS splicing, that protects Caenorhabditis elegans and human genes against DNA-transposon-mediated disruption by excising these TEs from host mRNAs. SOS splicing, which seems to operate independently of the spliceosome, is a pattern-recognition system triggered by the base-pairing of inverted terminal repeat elements, which are a defining feature of DNA transposons. We identify three factors required for SOS splicing in both C.elegans and human cells: AKAP17A, which binds TE-containing mRNAs; the RNA ligase RTCB; and CAAP1, which bridges RTCB and AKAP17A to allow RTCB to ligate mRNA fragments generated by TE excision. We propose that SOS splicing is a previously undescribed conserved and RNA-structure-directed mode of mRNA splicing, and that an identified function of SOS splicing is to genetically buffer animals from the deleterious effects of DNA-transposon-mediated gene perturbation.

DOI: 10.1038/s41586-025-09853-8

Source: https://www.nature.com/articles/s41586-025-09853-8