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Genome editing demonstrates that the -5 kb Nanog enhancer regulates Nanog expression by modulating RNAPII initiation and/or recruitment

ABSTRACT: Genome editing demonstrates that the -5 kb Nanog enhancer regulates Nanog expression by modulating RNAPII initiation and/or recruitment

PROVIDER: PRJNA602460 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10917037.fastq.gz	Fastqsanger.gz
	SRR10917037_1.fastq.gz	Fastqsanger.gz
	SRR10917037_2.fastq.gz	Fastqsanger.gz
	SRR10917038_1.fastq.gz	Fastqsanger.gz
	SRR10917038_2.fastq.gz	Fastqsanger.gz

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Genome editing demonstrates that the -5 kb Nanog enhancer regulates Nanog expression by modulating RNAPII initiation and/or recruitment.

Project description:Transcriptional enhancers have been defined by their ability to operate independent of distance and orientation in plasmid-based reporter assays of gene expression. At present, histone marks are used to identify and define enhancers but do not consider the endogenous role of an enhancer in the context of native chromatin. We employed a combination of genomic editing, single cell analyses, and sequencing approaches to investigate a Nanog-associated cis-regulatory element, which has been reported by others to be either an alternative promoter or a super-enhancer. We first demonstrate both distance and orientation independence in native chromatin, eliminating the issues raised with plasmid-based approaches. We next demonstrate that the dominant super-enhancer modulates Nanog globally and operates by recruiting and/or initiating RNA Polymerase II. Our studies have important implications to how transcriptional enhancers are defined and how they regulate gene expression.

| S-EPMC7948488 | biostudies-literature

Genome editing demonstrates that the -5 kb Nanog enhancer regulates Nanog expression by modulating RNAPII initiation and/or recruitment

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-07 | GSE143993 | GEO

Defining a critical Nanog enhancer using chromatin-focused approaches identifies RNAPII recruitment as required for expression [-5delRNASeq]

Project description:Transcriptional enhancers have been defined by their ability to operate independent of distance and orientation in plasmid reporters rather than native chromatin. We employed a combination of approaches to investigate the Nanog locus in mouse embryonic stem cells (ESCs) and an associated cis regulatory element (CRE) which may operate as either a super-enhancer (SE) or alternative promoter. We establish this element is a SE within chromatin using distance- and orientation-independence as criteria, and that it regulates Nanog by recruiting and/or initiating RNA Polymerase II. Our work highlights that enhancers can regulate gene expression through a diverse set of mechanisms.

2020-12-07 | GSE143959 | GEO

Defining a critical Nanog enhancer using chromatin-focused approaches identifies RNAPII recruitment as required for expression [-5delRNASeq]

Project description:Defining a critical Nanog enhancer using chromatin-focused approaches identifies RNAPII recruitment as required for expression [-5delRNASeq]

| PRJNA602333 | ENA

Defining a critical Nanog enhancer using chromatin-focused approaches identifies RNAPII recruitment as required for expression [ATAC-Seq]

Project description:Transcriptional enhancers have been defined by their ability to operate independent of distance and orientation in plasmid reporter assays, rather than within native chromatin. We employed a combination of approaches to investigate the Nanog locus in mouse embryonic stem cells (ESCs) and an associated cis regulatory element (CRE) which may operate as a super-enhancer (SE) or alternative promoter. We establish the element is a SE within chromatin using distance- and orientation-independence as criteria. We next demonstrate this SE regulates Nanog by recruiting and/or initiating RNA Polymerase II. Our work highlights that enhancers likely operate through a diverse set of mechanisms.

2020-12-07 | GSE149531 | GEO

Defining a critical Nanog enhancer using chromatin-focused approaches identifies RNAPII recruitment as required for expression [CUT&Tag]

2020-12-07 | GSE143991 | GEO

Defining a critical Nanog enhancer using chromatin-focused approaches identifies RNAPII recruitment as required for expression [ATAC-Seq]

Project description:Defining a critical Nanog enhancer using chromatin-focused approaches identifies RNAPII recruitment as required for expression [ATAC-Seq]

| PRJNA628990 | ENA

Defining a critical Nanog enhancer using chromatin-focused approaches identifies RNAPII recruitment as required for expression [CUT&Tag]

Project description:Defining a critical Nanog enhancer using chromatin-focused approaches identifies RNAPII recruitment as required for expression [CUT&Tag]

| PRJNA602469 | ENA

TCERG1 regulates alternative splicing of Bcl-x gene by modulating the rate of RNAPII transcription

Project description:Complex functional coupling exists between transcriptional elongation and pre-mRNA alternative splicing. Pausing sites and changes in the rate of transcription by RNAPII may therefore have a fundamental impact in the regulation of alternative splicing. Here, we show that the elongation and splicing-related factor TCERG1 regulates alternative splicing of the apoptosis gene Bcl-x in a promoter-dependent manner. TCERG1 promotes the splicing of the short isoform of Bcl-x (Bcl-xs) through the SB1 regulatory element located in the first half of exon 2. Consistent with these results, we show evidence for in vitro and in vivo interaction of TCERG1 with the Bcl-x pre-mRNA. Transcription profile analysis reveals that the RNA sequences required for the effect of TCERG1 on Bcl-x alternative splicing coincide with a putative polymerase pause site. Furthermore, TCERG1 modifies the impact of a slow polymerase on Bcl-x alternative splicing. In support of a role for an elongation mechanism in the transcriptional control of Bcl-x alternative splicing, we found that TCERG1 modifies the amount of pre-mRNAs generated at distal regions of the endogenous Bcl-x. Most importantly, TCERG1 affects the rate of RNAPII transcription of endogenous human Bcl-x. We propose that TCERG1 modulates the elongation rate of RNAPII to relieve pausing, thereby activating the pro-apoptotic Bcl-xS 5’ splice site. ChIP-Seq

2012-01-12 | E-GEOD-33716 | biostudies-arrayexpress

A dual role for H2A.Z.1 in modulating Initiating and Elongating RNAPII dynamics

Project description:RNA Polymerase II (RNAPII) pausing immediately downstream of the transcription start site (TSS) is a critical rate limiting step for the induction of most metazoan genes. During pause-release, RNAPII encounters a highly conserved +1 H2A.Z nucleosome, yet how this histone variant contributes to transcription is poorly understood. Here, using an inducible protein degron system combined with genomic approaches and live cell super-resolution microscopy, we show that H2A.Z.1 modulates RNAPII dynamics across most genes in murine embryonic stem cells (ESCs). Our quantitative analysis shows that H2A.Z.1 slows the rate of RNAPII pause release and consequently impacts Negative Elongation Factor (NELF) dynamics as well as nascent transcription. Consequently, H2A.Z.1 also impacts re-loading of the Pre-Initiation Complex (PIC) components TFIIB and TBP. Together, this work provides a critical mechanistic link between H2A.Z.1 and the proper induction of mammalian gene expression programs by regulating RNAPII dynamics and pause release.

2021-04-03 | GSE143737 | GEO

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