RNA helicases orchestrate proofreading mechanisms that facilitate accurate intron removal from pre-mRNAs. How these activities are recruited to spliceosome/pre-mRNA complexes remains poorly understood. In this issue of Genes & Development, Zhang and colleagues (pp. 968–983) combine biochemical experiments with AI-based structure prediction methods to generate a model for the interaction between SF3B1, a core splicing factor essential for the recognition of the intron branchpoint, and SUGP1, a protein that bridges SF3B1 with the helicase DHX15. Interaction with SF3B1 exposes the G-patch domain of SUGP1, facilitating binding to and activation of DHX15. The model can explain the activation of cryptic 3′ splice sites induced by mutations in SF3B1 or SUGP1 frequently found in cancer.

中文翻译：

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AI 辅助 RNA 剪接校对

RNA 解旋酶协调校对机制，促进从前 mRNA 中准确去除内含子。这些活性如何被招募到剪接体/前 mRNA 复合物中仍然知之甚少。在本期《基因与发育》中，Zhang 及其同事（第 968-983 页）将生化实验与基于人工智能的结构预测方法相结合，生成了 SF3B1 之间相互作用的模型，SF3B1 是识别内含子分支点所必需的核心剪接因子和 SUGP1，一种将 SF3B1 与解旋酶 DHX15 连接起来的蛋白质。与 SF3B1 的相互作用暴露了 SUGP1 的 G-patch 结构域，促进与 DHX15 的结合和激活。该模型可以解释癌症中常见的 SF3B1 或 SUGP1 突变诱导的隐秘 3' 剪接位点的激活。