Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Interplay between FACT subunit SPT16 and TRIM33 can remodel chromatin at macrophage distal regulatory elements [ChIP-seq]

ABSTRACT: Although the advances in genome-wide approaches have elucidated the functions of macrophage-specific distal regulatory elements in transcriptional responses, chromatin structures associated with PU.1 priming and the underlying mechanisms of action of these cis-acting sequences are not characterized. Here, we show that, in macrophages, FACT subunit SPT16 can bind to positioned nucleosomes directly flanking PU.1-bound sites at previously uncharacterized distal regulatory elements located near genes essential for macrophage development and functions. SPT16 can interact with the transcriptional co-regulator TRIM33 and binds to half of these sites in a TRIM33 dependent manner. Using the Atp1b3 locus as a model, we show that FACT binds to two positioned nucleosomes surrounding a TRIM33/PU.1-bound site in a region, located 35kb upstream the Atp1b3 TSS, that interact with the Atp1b3 promoter. At this -35kb region, TRIM33 deficiency leads to FACT release, loss of the two positioned nucleosomes, RNA Pol II recruitment and bidirectional transcription. These modifications are associated with higher levels of FACT binding at the Atp1b3 promoter, an increase of RNA Pol II recruitment and an increased expression of Atp1b3 in Trim33-/- macrophages. Thus, sequestering of SPT16/FACT by TRIM33 at PU.1-bound distal regions might represent a new regulatory mechanism for RNA Pol II recruitment and transcription output in macrophages.

ORGANISM(S): Mus musculus

PROVIDER: GSE117333 | GEO | 2019/08/06

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Interplay between FACT subunit SPT16 and TRIM33 can remodel chromatin at macrophage distal regulatory elements [ATAC-seq]

Project description:Although the advances in genome-wide approaches have elucidated the functions of macrophage-specific distal regulatory elements in transcriptional responses, chromatin structures associated with PU.1 priming and the underlying mechanisms of action of these cis-acting sequences are not characterized. Here, we show that, in macrophages, FACT subunit SPT16 can bind to positioned nucleosomes directly flanking PU.1-bound sites at previously uncharacterized distal regulatory elements located near genes essential for macrophage development and functions. SPT16 can interact with the transcriptional co-regulator TRIM33 and binds to half of these sites in a TRIM33 dependent manner. Using the Atp1b3 locus as a model, we show that FACT binds to two positioned nucleosomes surrounding a TRIM33/PU.1-bound site in a region, located 35kb upstream the Atp1b3 TSS, that interact with the Atp1b3 promoter. At this -35kb region, TRIM33 deficiency leads to FACT release, loss of the two positioned nucleosomes, RNA Pol II recruitment and bidirectional transcription. These modifications are associated with higher levels of FACT binding at the Atp1b3 promoter, an increase of RNA Pol II recruitment and an increased expression of Atp1b3 in Trim33-/- macrophages. Thus, sequestering of SPT16/FACT by TRIM33 at PU.1-bound distal regions might represent a new regulatory mechanism for RNA Pol II recruitment and transcription output in macrophages.

2019-08-06 | GSE132922 | GEO

Cryptic transcription is the primary driving force for nucleosome instability in Spt16 mutant cells

Project description:FACT consists of two essential subunits Spt16 and Pob3 and is a histone chaperone. Depletion of Spt16 using a an spt16 mutant results in a global alteration of nucleosome positions as well as aberrant transcription. Here we show that the majority of nucleosomal changes at gene body upon Spt16 depletion are independent of gene activity, but correlates with cryptic gene transcription and are suppressed by inhibition of RNA Polymerase II activities. In addition, A small fraction of nucleosomal changes is resistant to Pol II inhibition, and Spt16 is enriched at this subgroup of nucleosomes. Moreover, nucleosomes surrounding the initiation sites of cryptic transcription in the spt16 mutant cells are more dynamic than other regions. These results support a model that Spt16 maintains nucleosome stability locally to inhibit the initiation from cryptic transcription, which that once initiated drives additional nucleosome loss upon Spt16 depletion.

2016-05-05 | GSE66215 | GEO

tRNA pool analysis of S. cerevisiae using tRNA-HySeq

Project description:For a typical RNA polymerase (pol) II transcribed budding yeast gene, the 5' -end is characterized by a nucleosome-free region (NFR) immediate upstream of the transcription start site (TSS), flanked by two well-positioned nucleosomes (-1 and +1) containing H2A.Z. A similar arrangement of nucleosomes containing H2A.Z is found on the genes transcribed by pol III, which reside in the NFR actively maintained by the chromatin remodeling complexes. We did genome-wide MNase-seq and ChIP-seq experiments to study the nucleosome arrangement near pol III transcribed genes. We also measured the levels of different tRNAs in the tRNA pool of the wild type and Spt16 mutant (*spt16-197*) cells using tRNA-HySeq method. Although, it is difficult to measure the primary transcripts of tRNA due to their quick processing and the sequence degeneracy of the tRNA isogenes; a comparison of the wild type and Spt16 mutant showed both increase or decrease of tRNA transcripts. The result suggest that Spt16 may not be necessary for the transcription per se of tRNA genes.

2023-12-31 | GSE109527 | GEO

Genome-wide Localization of Mot1, Spt16, and Nucleosomes in mot1, spt16, and mot1 spt16 cells

Project description:Mot1 is a conserved and essential Swi2/Snf2 ATPase that can remove TATA-binding protein (TBP) from DNA using ATP hydrolysis, and in so doing exerts global effects on transcription. Spt16 is also essential and functions globally in transcriptional regulation as a component of the FACT histone chaperone complex. Here we demonstrate that Mot1 and Spt16 regulate a largely overlapping set of genes in Saccharomyces cerevisiae. As expected, Mot1 was found to control TBP levels at co-regulated promoters. In contrast, Spt16 did not affect TBP recruitment. On a global scale, Spt16 was required for Mot1 promoter localization, and Mot1 also affected Spt16 localization to genes. Interestingly, we find that Mot1 has an unanticipated role in establishing or maintaining the occupancy and positioning of nucleosomes at the 5’ ends of genes. Spt16 has a broad role in regulating chromatin organization in gene bodies, including those nucleosomes affected by Mot1. These results suggest that the large-scale overlap in Mot1 and Spt16 function arises from a combination of both their unique and shared functions in transcription complex assembly and chromatin structure regulation.

2016-05-16 | GSE80234 | GEO

Genome-wide Localization of Mot1, Spt16, and Nucleosomes in mot1, spt16, and mot1 spt16 cells

Project description:Mot1 is a conserved and essential Swi2/Snf2 ATPase that can remove TATA-binding protein (TBP) from DNA using ATP hydrolysis, and in so doing exerts global effects on transcription. Spt16 is also essential and functions globally in transcriptional regulation as a component of the FACT histone chaperone complex. Here we demonstrate that Mot1 and Spt16 regulate a largely overlapping set of genes in Saccharomyces cerevisiae. As expected, Mot1 was found to control TBP levels at co-regulated promoters. In contrast, Spt16 did not affect TBP recruitment. On a global scale, Spt16 was required for Mot1 promoter localization, and Mot1 also affected Spt16 localization to genes. Interestingly, we find that Mot1 has an unanticipated role in establishing or maintaining the occupancy and positioning of nucleosomes at the 5â ends of genes. Spt16 has a broad role in regulating chromatin organization in gene bodies, including those nucleosomes affected by Mot1. These results suggest that the large-scale overlap in Mot1 and Spt16 function arises from a combination of both their unique and shared functions in transcription complex assembly and chromatin structure regulation. ChIP was performed for Spt16-myc in WT cells and mot1-42 cells in duplicate with input DNA from WT as control. ChIP was performed for Mot1-myc in WT cells and spt16-197 cells in dublicate with input DNA from WT as control. Micrococcal nuclease digested chromatin from WT, mot1-42, spt16-197, and mot1-42 spt16-197 cells were immunoprecipitated with H3 antibody in duplicate. All samples were sequenced by Illumina MiSeq.

2016-05-16 | E-GEOD-80234 | biostudies-arrayexpress

Spatial regulation of transcription and histone occupancy by histone chaperones FACT and Spt6

Project description:The FACT complex and Spt6 are conserved histone chaperones that are recruited to the open reading frames of transcribed genes. In this study, we provide evidence that FACT interaction with acetylated H3 tail is important for its localization to the coding sequences. Pol II CTD kinase Kin28 additionally stimulates FACT recruitment to a subset of genes. Pol II occupancies in the 5’ ends of transcribed genes are greatly reduced on depleting FACT, whereas reduced occupancies at the 3’ ends were observed upon Spt6 depletion indicating that these factors modulate Pol II progression through distinct regions of transcribed coding sequences. While FACT is largely responsible for reassembling histones, we uncover a role for Spt6 in promoting histone eviction in addition to widely-accepted role for Spt6 in histone reassembly. Consistent with their localization in the coding regions, simultaneously impairing FACT and Spt6 function severely dampens histone eviction and impairs transcription genome-wide. ChIP-chip experiments to measure Spt16 occupancies in WT and kin28as mutant, as well Rpb3 and histone H3 occupancies in undepleted or depleted cells for Spt16 and Spt6, and also in the strain lacking Spt6 tandem SH2 domain

2018-05-21 | GSE69642 | GEO

Interplay between FACT subunit SPT16 and TRIM33 can remodel chromatin at macrophage distal regulatory elements

Project description:Interplay between FACT subunit SPT16 and TRIM33 can remodel chromatin at macrophage distal regulatory elements

| PRJNA549472 | ENA

Interplay between FACT subunit SPT16 and TRIM33 can remodel chromatin at macrophage distal regulatory elements [ChIP-seq]

Project description:Interplay between FACT subunit SPT16 and TRIM33 can remodel chromatin at macrophage distal regulatory elements [ChIP-seq]

| PRJNA481772 | ENA

Interplay between FACT subunit SPT16 and TRIM33 can remodel chromatin at macrophage distal regulatory elements [ATAC-seq]

Project description:Interplay between FACT subunit SPT16 and TRIM33 can remodel chromatin at macrophage distal regulatory elements [ATAC-seq]

| PRJNA549476 | ENA

The transcriptional cofactor TRIM33 prevents apoptosis in B lymphoblastic leukemia by deactivating a single enhancer [ChIP-Seq]

Project description:Most mammalian transcription factors and cofactors occupy thousands of genomic sites and modulate the expression of large gene networks to implement their biological functions. In this study, we describe an exception to this paradigm. TRIM33 is identified here as a lineage dependency in B cell neoplasms and is shown to perform this essential function by associating with a single cis element. ChIP-seq analysis of TRIM33 in murine B cell leukemia revealed a preferential association with two lineage-specific enhancers that harbor an exceptional density of motifs recognized by the PU.1 transcription factor. TRIM33 is recruited to these elements by PU.1, yet acts to antagonize PU.1 function. One of the PU.1/TRIM33 co-occupied enhancers is upstream of the pro-apoptotic gene Bim, and deleting this enhancer renders TRIM33 dispensable for leukemia cell survival. These findings reveal an essential role for TRIM33 in preventing apoptosis in B lymphoblastic leukemia by interfering with enhancer-mediated Bim activation. ChIP-Seq for Trim33, Pu.1 and histone modification marks in different types of leukemia cells

2015-04-06 | E-GEOD-66233 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data