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TRIM71 represses let-7 miRNA expression and activity via two independent molecular mechanisms

ABSTRACT: TRIM71 represses let-7 miRNA expression and activity via two independent molecular mechanisms

PROVIDER: PRJNA686975 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13299732_1.fastq.gz	Fastqsanger.gz
	SRR13299732_2.fastq.gz	Fastqsanger.gz
	SRR13299733_1.fastq.gz	Fastqsanger.gz
	SRR13299733_2.fastq.gz	Fastqsanger.gz
	SRR13299734_1.fastq.gz	Fastqsanger.gz

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TRIM71 represses let-7 miRNA expression and activity via two independent molecular mechanisms

Project description:Let-7 is a well-known pro-differentiation and tumor suppressor miRNA. TRIM71/LIN-41 was the first identified let-7 target, and it is a conserved stem cell-specific RNA-binding protein with an essential function in embryonic development and a proposed oncogenic role in several cancer types, such as hepatocellular carcinoma. Previous studies suggest a role for TRIM71 in miRNA regulation, since major changes have been observed in the miRNome of TRIM71-defiecient ESCs, and TRIM71 is able to interact with several proteins involved in the miRNA pathway.

2021-09-09 | GSE163635 | GEO

A TRIM71 binding long noncoding RNA Trincr1 represses FGF/ERK signaling in embryonic stem cells

Project description: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 identified 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 led to the upregulation of phosphorylated ERK and ERK pathway target genes and the decrease of ESC self-renewal, while knocking down Trim71 completely rescued the defects of Trincr1 knockout. Furthermore, ectopic expression of Trincr1 repressed FGF/ERK signaling and the self-renewal of neural progenitor cells. Together, this study reveals novel regulators in FGF/ERK signaling pathway and highlights lncRNA as an important player in cell signaling network to coordinate cell fate specification.

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miRNA sequencing of Trim71 conditional ("WT") and Trim71 KO mES cells

Project description:We report that Trim71 mutation induces significant changes in the global expression profile of miRNAs in undifferentiated mES cells, rendering the cells prone to differentiation.

2015-10-01 | GSE62509 | GEO

The stem cell-specific protein TRIM71 inhibits maturation and activity of the pro-differentiation miRNA let-7 via two independent molecular mechanisms.

Project description:The stem cell-specific RNA-binding protein TRIM71/LIN-41 was the first identified target of the pro-differentiation and tumor suppressor miRNA let-7. TRIM71 has essential functions in embryonic development and a proposed oncogenic role in several cancer types, such as hepatocellular carcinoma. Here, we show that TRIM71 regulates let-7 expression and activity via two independent mechanisms. On the one hand, TRIM71 enhances pre-let-7 degradation through its direct interaction with LIN28 and TUT4, thereby inhibiting let-7 maturation and indirectly promoting the stabilization of let-7 targets. On the other hand, TRIM71 represses the activity of mature let-7 via its RNA-dependent interaction with the RNA-Induced Silencing Complex (RISC) effector protein AGO2. We found that TRIM71 directly binds and stabilizes let-7 targets, suggesting that let-7 activity inhibition occurs on active RISCs. MiRNA enrichment analysis of several transcriptomic datasets from mouse embryonic stem cells and human hepatocellular carcinoma cells suggests that these let-7 regulatory mechanisms shape transcriptomic changes during developmental and oncogenic processes. Altogether, our work reveals a novel role for TRIM71 as a miRNA repressor and sheds light on a dual mechanism of let-7 regulation.

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mRNA sequencing of Trim71 conditional ("WT") and Trim71 KO mES cells

Project description:We report that Trim71 mutation does not lead to significant changes within the core regulatory network of mES cells, however, there is an upregulation of specific genes involved in neural differentiation. We thus conclude that Trim71 KO mES cells are poised for differentiation.

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NuRD independent Mi2 activity represses ectopic gene expression during neuronal maturation

Project description:NuRD independent Mi2 activity represses ectopic gene expression during neuronal maturation

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Studies on Trim71 in mouse embryonic stem cells

Project description:We studies on Trim71 regulates mouse embryonic stem cells by identifying the transcriptome-wide RNA targets of Trim71. Moreover, through inhibiting specific Trim71:mRNA interactions, we determined how Trim71 modulate miRNA activity in mouse embryonis cell cells

2021-02-23 | GSE138284 | GEO

Studies on a hydrocephalus-causing mutation on Trim71

Project description:We studies on how a hydrocephalus-causing mutation (R783H) on Trim71 alters Trim71's substrate mRNA binding

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The RNA hairpin binder TRIM71 modulates alternative splicing by repressing Mbnl1

Project description:We demonstrate that global effects of TRIM71 on the cellular transcriptome of mouse embryonic stem cells (mESCs) are largely attributable to its RNA binding activity, and map the transcriptome-wide targets of wild-type TRIM71, NHL domain mutant TRIM71, and RING domain mutant TRIM71.

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Project description:We studies on how a hydrocephalus-associated mutation (R595H) on Trim71 alters Trim71's substrate mRNA binding

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