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聚烯 (GR) 与关键的压力颗粒因子相互作用,促进其组装到细胞质内含物中

Jinyoung Park¹, Yanwei Wu¹, Wei Shao¹

¹Department of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.

|July 20, 2023

概括

C9orf72的重复扩张会导致前性痴呆症 (FTD) 和肌性侧面硬化症 (ALS). 通过与G3BP1和m6A修饰RNA相互作用而形成的多元GR合,促进疾病.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
遗传学遗传学是一个

背景情况:

C9orf72重复扩张是前性痴呆症 (FTD) 和肌性侧面硬化症 (ALS) 的主要遗传原因.
有毒的多分子GR蛋白质形成细胞质内含物,隔离RNA结合蛋白质并破坏细胞功能.
控制聚烯 (GR) 纳入形成的机制在很大程度上是未知的.

研究的目的:

调查影响C9orf72-相关FTD/ALS中的多元 (GR) 纳入形成的因素.
为了确定参与C9orf72 FTD/ALS.病变发生的关键蛋白质和RNA相互作用.

主要方法:

研究了poly (GR) 与应力颗粒 (SG) 组件的相互作用,特别是G3BP1.1.
分析了N extsuperscript{6}-methyladenosine (m6A) 修饰的mRNA和YTHDF蛋白在多种GR纳入形成中的同定位和作用.
从c9FTD/ALS小鼠模型和患者的大脑组织中检查了多样性 (GR) 入.

主要成果:

聚基透到SG形成所必需的蛋白质-RNA相互作用网络中.
一个关键的SG组装因子G3BP1对于聚合物 (GR) 纳入形成至关重要.
m6A修饰的mRNA和YTHDF蛋白质通过将RNA纳入这些纳入物来促进多样性 (GR) 纳入形成.

结论:

通过与G3BP1和m6A修饰RNA机器的相互作用来调节Poly(GR) 纳入形成.
准与G3BP1或YTHDF1的多基因相互作用,或降低多基因水平,是c9FTD/ALS的潜在治疗策略.
了解这些分子相互作用为C9orf72 FTD/ALS.的神经退行性机制提供了洞察力.

关键词:

科普:分子生物学分子生物学科普:神经科学是什么意思在 G3BP1/2 这些蛋白质是YTHDF蛋白质.骨髓缩侧面硬化症 (ALS) 是一种染色体9 开放的阅读框架 72 细胞质多分子 (GR) 入.双重复蛋白质的蛋白质重复蛋白质.前性痴呆症前性痴呆症液态-液态相隔离方法液态相隔离方法 m6A修饰的RNAs可以被使用.

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