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酵母TIA1与Npl3协调,在饥饿期间促进ATG1的翻译
Shree Padma Metur1, Xinxin Song2, Sophie Mehta1
1Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109-2216, USA; Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Cell reports
|February 15, 2025
概括
RNA结合蛋白Npl3和Pub1通过控制ATG1mRNA的输出和翻译来调节自. 这种机制在营养饥饿期间对细胞生存至关重要,并且在癌细胞中被保存.
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:
- 在营养缺乏的情况下,宏自/自对细胞生存至关重要.
- Atg1激酶对于有效的自诱导和执行至关重要.
- RNA结合蛋白 (RBPs) 越来越多地被认为是它们在自相关基因的转录后调节中的作用,包括ATG1.
研究的目的:
- 识别与ATG1未翻译区域 (UTR) 相互作用的RBP.
- 阐明RBPs调节ATG1表达和自的机制.
- 研究这些RBP的哺乳动物同类在癌细胞自中的作用.
主要方法:
- 在体外拉下测试以确定与ATG1 UTRs结合的RBP.
- 对mRNA出口和翻译效率的分析.
- 西方涂抹测试用于评估非小细胞肺癌 (NSCLC) 线的蛋白质表达.
主要成果:
- Npl3和Pub1被确定为RBP,在饥饿期间与ATG1的5'和3'UTR相互作用.
- Npl3和Pub1合作促进ATG1mRNA输出到细胞质和翻译.
- 哺乳动物Pub1和TIA1在血清饥饿期间在NSCLC细胞中增强ULK1蛋白表达和自.
结论:
- Npl3和Pub1是通过mRNA输出和翻译ATG1表达的关键调节者.
- 这种RBP介导的ATG1调节对于在营养缺乏期间维持自至关重要.
- 这些发现揭示了一种涉及哺乳动物RBP调节自的保存机制,这对癌症生物学有意义.
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