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A TRIM71 binding long noncoding RNA Trincr1 represses FGF/ERK signaling in embryonic stem cells
Nature Communications ( IF 14.7 ) Pub Date : 2019-03-25 , DOI: 10.1038/s41467-019-08911-w
Ya-Pu Li , Fei-Fei Duan , Yu-Ting Zhao , Kai-Li Gu , Le-Qi Liao , Huai-Bin Su , Jing Hao , Kun Zhang , Na Yang , Yangming Wang

Long noncoding RNAs (lncRNAs) have emerged as important components of gene regulatory network in embryonic stem cells (ESCs). However, the function and molecular mechanism of lncRNAs are still largely unknown. Here we identifies Trincr1 (TRIM71 interacting long noncoding RNA 1) lncRNA that regulates the FGF/ERK signaling and self-renewal of ESCs. Trincr1 is exported by THOC complex to cytoplasm where it binds and represses TRIM71, leading to the downregulation of SHCBP1 protein. Knocking out Trincr1 leads to the upregulation of phosphorylated ERK and ERK pathway target genes and the decrease of ESC self-renewal, while knocking down Trim71 completely rescues the defects of Trincr1 knockout. Furthermore, ectopic expression of Trincr1 represses FGF/ERK signaling and the self-renewal of neural progenitor cells (NPCs). Together, this study highlights lncRNA as an important player in cell signaling network to coordinate cell fate specification.



中文翻译:

TRIM71结合长非编码RNA Trincr1抑制胚胎干细胞中的FGF / ERK信号传导。

长的非编码RNA(lncRNA)已成为胚胎干细胞(ESC)中基因调控网络的重要组成部分。但是,lncRNAs的功能和分子机制仍是未知之数。在这里,我们识别Trincr1(TR IM71nteracting长ÑÇ oding - [R NA 1)调控FGF / ERK信号传导和ESC自我更新的lncRNA。Trincr1通过THOC复合物输出到细胞质,在那里它结合并抑制TRIM71,从而导致SHCBP1蛋白的下调。敲除Trincr1导致磷酸化ERK和ERK通路靶基因的上调和ESC自我更新的减少,而敲除Trim71则完全可以挽救Trincr1敲除的缺陷。此外,Trincr1的异位表达抑制FGF / ERK信号传导和神经祖细胞(NPC)的自我更新。总之,这项研究突出了lncRNA在协调细胞命运规范的细胞信号网络中的重要作用。

更新日期:2019-03-25
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