RNA剪接
生物
计算生物学
RNA结合蛋白
剪接
融合蛋白
肌萎缩侧索硬化
遗传学
核糖核酸
细胞生物学
基因
疾病
医学
病理
重组DNA
作者
Oscar G. Wilkins,Max Z. Y. J. Chien,Josette J Wlaschin,Simone Barattucci,Peter Harley,Francesca Mattedi,Puja R. Mehta,Maria Pisliakova,Eugeni Ryadnov,Matthew J. Keuss,David Thompson,Holly Digby,Lea Knez,Rebecca L. Simkin,Juan Antinao Díaz,Matteo Zanovello,Anna‐Leigh Brown,Annalucia Darbey,Rajvinder Karda,Elizabeth Fisher
出处
期刊:Science
[American Association for the Advancement of Science]
日期:2024-10-03
卷期号:386 (6717): 61-69
被引量:6
标识
DOI:10.1126/science.adk2539
摘要
Loss of function of the RNA-binding protein TDP-43 (TDP-LOF) is a hallmark of amyotrophic lateral sclerosis (ALS) and other neurodegenerative disorders. Here we describe TDP-REG, which exploits the specificity of cryptic splicing induced by TDP-LOF to drive protein expression when and where the disease process occurs. The SpliceNouveau algorithm combines deep learning with rational design to generate customizable cryptic splicing events within protein-coding sequences. We demonstrate that expression of TDP-REG reporters is tightly coupled to TDP-LOF in vitro and in vivo. TDP-REG enables genomic prime editing to ablate the UNC13A cryptic donor splice site specifically upon TDP-LOF. Finally, we design TDP-REG vectors encoding a TDP-43/Raver1 fusion protein that rescues key pathological cryptic splicing events, paving the way for the development of precision therapies for TDP43-related disorders.
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