RIOK3调解了40S核糖体的降解过程
Zixuan Huang1, Frances F Diehl2, Mengjiao Wang1
1Minhang Hospital & Institutes of Biomedical Sciences, Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Fudan University Shanghai, China.
Molecular cell
|February 13, 2025
概括
饥饿会触发40S核糖体的选择性降解,通过RNF10的无处不在和RIOK3.3的识别. 这一途径揭示了在细胞应激期间维持核糖体平衡的机制.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 细胞保持核糖体恒常性,以适应.
- 压力期间的核糖体降解是不太了解的.
- 需要选择性去除核糖体子单元的机制.
研究的目的:
- 阐明饥饿期间40S核糖体降解的机制.
- 确定参与压力诱导的核糖体周转的关键蛋白质.
- 将无处不在与核糖体平衡调节联系起来.
主要方法:
- 使用E3结合酶RNF10进行泛基化试验.
- 用非典型的激酶RIOK3.3进行蛋白与蛋白相互作用研究.
- 电子显微镜 (cryo-EM) 用于结构分析.
- 对18S rRNA降解中间体的分析.
主要成果:
- 饥饿诱导了RNF10的40S核糖体无处不在.
- RIOK3通过一种与ubiquitin相互作用的基因识别了无处不在的40S核糖体.
- 在饥饿期间,RIOK3对于40S核糖体降解至关重要.
- 化EM揭示了由RIOK3.3启动的渐进式18SrRNA衰变.
结论:
- 定义了压力诱导的40S核糖体降解的新途径.
- 泛基化和RIOK3对于选择性的核糖体子单元去除至关重要.
- 这种机制直接将无处不在与核糖体平衡维持联系起来.
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