The miR-26 family regulates neural differentiation-associated microRNAs and mRNAs by directly targeting REST
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ABSTRACT:
PROVIDER: PRJNA720669 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14189708.fastq.gz | Fastqsanger.gz | |||
| SRR14189709.fastq.gz | Fastqsanger.gz | |||
| SRR14189710.fastq.gz | Fastqsanger.gz | |||
| SRR14189711.fastq.gz | Fastqsanger.gz | |||
| SRR14189712.fastq.gz | Fastqsanger.gz |
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Project description:Our data identify the miR-26 family as a trigger of a self-amplifying system essential for neural differentiation that acts upstream REST-controlled miRs and initiate a neuronal gene expression program.
2021-04-09 | GSE171727 | GEO
Project description:Repressor element 1-silencing transcription factor (REST) plays a crucial role in the differentiation of neural progenitor cells (NPCs). C-terminal domain small phosphatases (CTDSPs) are REST effector proteins that reduce RNA polymerase II activity on genes required for neurogenesis. miR-26b regulates neurogenesis in zebrafish by targeting ctdsp2 mRNA, but the molecular events triggered by this microRNA (miR) remain unknown. Here, we show in a murine embryonic stem cell differentiation paradigm that inactivation of miR-26 family members disrupts the formation of neurons and astroglia and arrests neurogenesis at the neural progenitor level. Furthermore, we show that miR-26 directly targets Rest, thereby inducing the expression of a large set of REST complex-repressed neuronal genes, including miRs required for induction of the neuronal gene expression program. Our data identify the miR-26 family as the trigger of a self-amplifying system required for neural differentiation that acts upstream of REST-controlled miRs.
| S-EPMC11443607 | biostudies-literature
Project description:Comamonas sp. 26 strain:26 Genome sequencing and assembly
| PRJNA402406 | ENA
Project description:Loss of REST function is seen in ~20% of breast cancers and is associated with a more aggressive phenotype and poor prognosis. Despite the frequent loss of REST, little is known about the role of REST in the molecular pathogenesis of breast cancer. We then utilized gene knockdown in MCF-7 cells in the presence or absence of steroid hormones estrogen and/ progesterone followed by RNA sequencing in an attempt to understand the tumor suppressor role of REST in breast cancer. We show that REST directly regulates CEMIP (cell migration-inducing and hyaluronan-binding protein, KIAA1199) and MMP24 (matrix metallopeptidase 24), genes known to have roles in invasion and metastasis. REST knockdown in breast cancer cells leads to significant upregulation of CEMIP and MMP24. In addition, we found REST binds to RE-1 sites (repressor element-1) within the genes and influences their transcription. Furthermore, we found that the estrogen receptor (ESR1) signaling pathway is activated in the absence of REST, regardless of hormone treatment. We demonstrate a critical role for the loss of REST in aggressive breast cancer pathogenesis and provide evidence for REST as an important diagnostic marker for personalized treatment plans.
2022-02-23 | GSE173857 | GEO
Project description:Cell epigenomics depends on the marks released by transcription factors operating via the assembly of complexes that induce focal changes of DNA and histone structure. Among these factors is REST, a repressor that, via its strong decrease, governs both neuronal and neural cell differentiation and specificity. REST operation on thousands of possible genes can occur directly or via indirect mechanisms including repression of other factors. In previous studies of gene down- and up-regulation, processes had been only partially investigated in neural cells. PC12 are well known neural cells sharing properties with neurons. In the widely used PC12 populations, low-REST cells coexist with few, spontaneous high-REST PC12 cells. High- and low-REST PC12 clones were employed to investigate the role and the mechanisms of the repressor action. Among 15,500 expressed genes we identified 1,770 target and non-target, RESTdependent genes. Functionally, these genes were found to operate in many pathways, from synaptic function to extracellular matrix. Mechanistically, downregulated genes were predominantly repressed directly by REST; up-regulated genes were mostly governed indirectly. Among other factors, Polycomb complexes cooperated with REST for down-regulation, Smad3 and Myod1 participated in up-regulation. In conclusion, we have highlighted that PC12 clones are a useful model to investigate REST, opening opportunities to development of epigenomic investigation.
2015-08-31 | GSE59946 | GEO
Project description:Namgyu Lee has participated in the experimental part of this project and she is a co-first author of the under-going manuscript. RE-1 silencing transcription factor (REST) is a transcriptional repressor with a role in regulating gene expression through binding to repressor element 1. We identified REST/NRSF-interacting proteins by proteomics-based analyses using the complementary mass spectrometry approach. Our interactome revealed 204 REST-interacting proteins. Among those proteins, nuclear proteins were mostly enriched reflecting nuclear localization of REST. The interaction networks of interactome indicated biological processes associated with mRNA processing, chromatin organization and transcription. Interactions of ALYREF, HnRNP M, HnRNP Q, NPM1, NCL, PARP1, HDAC5, TRIM28 and HMGA1 with REST were confirmed by co-immunoprecipitation. Using public microarray dataset, a highly significant overlaps were observed in differentially expressed transcripts following knockdown of REST and interacting proteins such as HDAC5, HMGA1 and TRIM28, suggesting that the REST might cross-talk with those transcription regulators to regulate transcription of shared target genes. Our interactomic study of REST implies novel cross-talks with transcription regulators by its associations with interacting proteins.
2018-10-25 | PXD003210 | Pride
Project description:Abstract - Huntingtin (Htt) protein interacts with many transcriptional regulators, with widespread disruption to the transcriptome in Huntington’s disease (HD) brought about by altered interactions with the mutant Htt (muHtt) protein. Repressor Element-1 Silencing Transcription Factor (REST) is a repressor whose association with Htt in the cytoplasm is disrupted in HD, leading to increased nuclear REST and concomitant repression of several neuronal-specific genes, including brain-derived neurotrophic factor (Bdnf). Here, we explored a wide set of HD dysregulated genes to identify direct REST targets whose expression is altered in a cellular model of HD but that can be rescued by knock-down of REST activity. We found many direct REST target genes encoding proteins important for nervous system development, including a cohort involved in synaptic transmission, at least two of which can be rescued at the protein level by REST knock-down. We also identified several microRNAs (miRNAs) whose aberrant repression is directly mediated by REST, including miR-137, which has not previously been shown to be a direct REST target in mouse. These data provide evidence of the contribution of inappropriate REST-mediated transcriptional repression to the widespread changes in coding and non-coding gene expression in a cellular model of HD that may affect normal neuronal function and survival.
2013-01-03 | GSE42107 | GEO
Project description:Comamonas sp. 26 transcriptome - Chisto_RNA_11
| PRJNA566532 | ENA
Project description:ENCODE ChIP-chip study using 8 diverse human cell lines; 4 of neural origin (NB69, KELLY, SHSY-5Y, U373) and 4 of non-neural origin (HeLa, HepG2, HEK293 and K562) and anti-REST/NRSF antibody (Santa Cruz Biotech; sc-25398 aka H290) to asses REST-genome interactions across 1% of the human genome used in the pilot phase of the ENCODE project. Additionally the REST binding profile in K562 cells that had been transfected with REST specific siRNA oligos (72h and 96h) were determined revealing genomic in vivo binding affinity hierarchies for REST. Additionally the REST binding profile in K562 cells that had been transfected with REST specific siRNA oligos (72h and 96h) were determined
2009-03-31 | E-TABM-660 | biostudies-arrayexpress
Project description:Cell epigenomics depends on the marks released by transcription factors operating via the assembly of complexes that induce focal changes of DNA and histone structure. Among these factors is REST, a repressor that, via its strong decrease, governs both neuronal and neural cell differentiation and specificity. REST operation on thousands of possible genes can occur directly or via indirect mechanisms including repression of other factors. In previous studies of gene down- and up-regulation, processes had been only partially investigated in neural cells. PC12 are well known neural cells sharing properties with neurons. In the widely used PC12 populations, low-REST cells coexist with few, spontaneous high-REST PC12 cells. High- and low-REST PC12 clones were employed to investigate the role and the mechanisms of the repressor action. Among 15,500 expressed genes we identified 1,770 target and non-target, RESTdependent genes. Functionally, these genes were found to operate in many pathways, from synaptic function to extracellular matrix. Mechanistically, downregulated genes were predominantly repressed directly by REST; up-regulated genes were mostly governed indirectly. Among other factors, Polycomb complexes cooperated with REST for down-regulation, Smad3 and Myod1 participated in up-regulation. In conclusion, we have highlighted that PC12 clones are a useful model to investigate REST, opening opportunities to development of epigenomic investigation. 4 samples have been analyzed: 2 replicates from wtPC12 clone and 2 replicates from the hrPC12 clones
2015-08-31 | E-GEOD-59946 | biostudies-arrayexpress