Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Temporal auto-regulation during PU.1 locus SubTAD formation

ABSTRACT: Temporal auto-regulation during PU.1 locus SubTAD formation

PROVIDER: PRJNA491721 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6730100.fastq.gz	Fastqsanger.gz
	SRR6730110.fastq.gz	Fastqsanger.gz
	SRR6730120.fastq.gz	Fastqsanger.gz
	SRR6730091.fastq.gz	Fastqsanger.gz
	SRR6730101.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 37

Similar Datasets

Temporal auto-regulation during PU.1 locus SubTAD formation (ChIP-seq)

Project description:Temporal auto-regulation during PU.1 locus SubTAD formation (ChIP-seq)

| PRJNA491722 | ENA

Temporal auto-regulation during PU.1 locus SubTAD formation (4C-seq)

Project description:Temporal auto-regulation during PU.1 locus SubTAD formation (4C-seq)

| PRJNA434257 | ENA

Temporal auto-regulation during PU.1 locus SubTAD formation (4C-seq)

Project description:Epigenetic control of gene expression occurs through discrete spatial chromosomal units called topologically associating domains (TADs), but the exact spatial requirements of most genes are unknown; this is of particular interest for genes involved in disease. We therefore applied high-resolution chromosomal conformation capture-sequencing to map the three-dimensional (3D) organization of the locus encoding the key myeloid transcription factor PU.1 in healthy monocytes and acute myeloid leukemia (AML) cells. We identified a dynamic ~75kb unit (SubTAD) as the genomic region in which spatial interactions between PU.1 gene regulatory elements occur during myeloid differentiation and are interrupted in AML. Within this SubTAD, initiating the spatial chromosomal interactions requires PU.1 auto-regulation and recruitment of the chromatin-adaptor protein LDB1 (LIM domain-binding protein 1). However, once formed, this SubTAD remains stable even when auto-regulation is impaired. Thus, our data support that PU.1 auto-regulation functions in a ‘hit-and-run’ manner, whereby it organizes chromosomal loops to create a transcriptionally active chromatin architecture.

2018-10-15 | GSE110683 | GEO

Temporal auto-regulation during PU.1 locus SubTAD formation (ChIP-seq)

Project description:Epigenetic control of gene expression occurs within discrete spatial chromosomal units called topologically associating domains (TADs), but the exact spatial requirements of most genes are unknown; this is of particular interest for genes involved in cancer. We therefore applied high-resolution chromosomal conformation capture-sequencing to map the three-dimensional (3D) organization of the human locus encoding the key myeloid transcription factor PU.1 in healthy monocytes and acute myeloid leukemia (AML) cells. We identified a dynamic ~75kb unit (SubTAD) as the genomic region in which spatial interactions between PU.1 gene regulatory elements occur during myeloid differentiation and are interrupted in AML. Within this SubTAD, proper initiation of the spatial chromosomal interactions requires PU.1 autoregulation and recruitment of the chromatin-adaptor protein LDB1 (LIM domain-binding protein 1). However, once these spatial interactions have occurred, LDB1 stabilizes them independently of PU.1 auto-regulation. Thus, our data support that PU.1 auto-regulates its expression in a ‘hit-and-run’ manner by initiating stable chromosomal loops that result in a transcriptionally active chromatin architecture.

2018-10-15 | GSE120142 | GEO

Temporal auto-regulation during PU.1 locus SubTAD formation

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

2018-10-15 | GSE120143 | GEO

Two distinct auto-regulatory loops operate at the Pu.1 locus in B cells and myeloid cells

Project description:The transcription factor PU.1 occupies a central role in controlling myeloid and early B cell development and its correct lineage-specific expression is critical for the differentiation choice of hematopoietic progenitors. However, little is known of how this tissue-specific pattern is established. We previously identified an upstream regulatory cis-element (URE) whose targeted deletion in mice decreases PU.1 expression and causes leukemia. We show here that the URE alone is insufficient to confer physiological PU.1 expression, but requires the cooperation with other, previously unidentified elements. Using a combination of transgenic studies, global chromatin assays and detailed molecular analyses we present evidence that Pu.1 is regulated by a novel mechanism involving cross-talk between different cis-elements together with lineage-restricted autoregulation. In this model, PU.1 regulates its expression in B cells and macrophages by differentially associating with cell-type specific transcription factors at one of its cis-regulatory elements to establish differential activity patterns at other elements. Two DNaseI hypersensitivity datasets; bone marrow derived-macrophages and Splenic CD19+IgM+ B cells were used to study PU.1 regulatory elements

2011-02-21 | E-GEOD-26550 | biostudies-arrayexpress

Two distinct auto-regulatory loops operate at the Pu.1 locus in B cells and myeloid cells

2011-02-21 | GSE26550 | GEO

The temporal transcriptomic signature of cartilage formation

Project description:The temporal transcriptomic signature of cartilage formation

| PRJEB60592 | ENA

PU.1

Project description:PU.1

| PRJNA344317 | ENA

Temporal dynamics of gene expression in Campylobacter jejuni biofilm formation

Project description:Temporal dynamics of gene expression in Campylobacter jejuni biofilm formation

| PRJNA1136887 | ENA