浙大校友一作Nature论文：新型RNA剪接系统——SOS剪接，在mRNA水平修复转座子的破坏

Core Viewpoint - The article discusses a novel RNA splicing system called SOS splicing, which actively repairs genetic information by excising DNA transposons from mRNA, thereby protecting gene function when traditional silencing mechanisms fail [2][15]. Group 1: Introduction to Transposable Elements - Transposable elements (TEs), also known as "jumping genes," are DNA sequences that can move or copy themselves within the genome, constituting a significant portion of various organisms' genomes (3%-80%) [1]. - The presence of TEs poses a threat to gene function, prompting the evolution of epigenetic systems to silence their expression and replication [1]. Group 2: Discovery of SOS Splicing - The research led by Dr. Zhao Longwen at Harvard Medical School identifies a new RNA splicing system, SOS splicing, which operates independently of the classical spliceosome [2][15]. - SOS splicing serves as an emergency response mechanism, recognizing and removing transposon sequences from host mRNA, thus attempting to restore protein expression and protect gene function [2]. Group 3: Mechanism of SOS Splicing - The SOS splicing system is triggered by a characteristic feature of DNA transposons, the inverted terminal repeat (ITR) sequence, which forms a "hairpin" structure in mRNA [11]. - Key components of this system include AKAP17A (the "scout" that recognizes mRNA with transposons), RTCB (the "repairer" that reconnects mRNA fragments), and CAAP1 (the "connector" that recruits RTCB) [12]. Group 4: Implications and Future Directions - The study reveals that SOS splicing provides a last line of defense for gene function when epigenetic silencing systems are compromised, highlighting the complexity of gene regulation [15]. - Although SOS splicing is efficient, it is not precise, often resulting in small mutations in repaired mRNA, yet it still allows for the production of functional proteins, offering survival advantages [18]. - The potential for medical applications exists, as understanding SOS splicing could lead to new gene therapy strategies to repair harmful mutations in human disease genes [18].