Genome-wide occupancy of chromatin remodeller SMARCAL1 and BRG1 in human cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA564931 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10097529_1.fastq.gz | Fastqsanger.gz | |||
| SRR10097529_2.fastq.gz | Fastqsanger.gz | |||
| SRR10097530_1.fastq.gz | Fastqsanger.gz | |||
| SRR10097530_2.fastq.gz | Fastqsanger.gz | |||
| SRR10097531_1.fastq.gz | Fastqsanger.gz |
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Project description:In this study we report genome wide occupancy of SMARCAL1 and BRG1 in control HeLa cells. Our analysis showed binding of these two remodellers on DNA damage response gene, chromatin remodellers, cell cycle and apoptosis regulating genes.
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2022-12-01 | E-MTAB-12452 | biostudies-arrayexpress
Project description:Pioneer transcription factors are able to recognise and bind their motif sequences in inaccessible or closed chromatin, and their ability to achieve this is required to establish new regulatory elements and transcriptional networks during development and cellular reprogramming. An essential feature of this pioneering activity is the transition from inaccessible chromatin to a nucleosome-depleted and accessible chromatin state typical of normal regulatory elements, and this is believed to facilitate further transcription factor binding events. However, the mechanisms by which many pioneer transcription factors achieve this remarkable feat remain elusive. Here we reveal that the pluripotency-associated pioneer factor OCT4 binds inaccessible chromatin to shape the chromatin accessibility, transcription factor co-binding and regulatory potential of thousands of distal regulatory elements in mouse embryonic stem cells, demonstrating that its pioneering activity is a feature of normal pluripotency, and not just reprogramming. The accessible chromatin formed at OCT4 binding sites relies on the chromatin remodelling factor BRG1, which is recruited to these sites by OCT4. The occupancy of BRG1 is then required to support OCT4/SOX2 co-binding and normal expression of the pluripotency-associated transcriptome, and this reliance on BRG1 reflects OCT4 binding dynamics during cellular reprograming and early mouse development. Together these observations reveal a distinct requirement for the chromatin remodelling factor BRG1 in shaping the pioneering activity of OCT4 and regulating the pluripotency network in embryonic stem cells.
2017-03-13 | GSE87821 | GEO
Project description:Pioneer transcription factors are able to recognise and bind their motif sequences in inaccessible or closed chromatin, and their ability to achieve this is required to establish new regulatory elements and transcriptional networks during development and cellular reprogramming. An essential feature of this pioneering activity is the transition from inaccessible chromatin to a nucleosome-depleted and accessible chromatin state typical of normal regulatory elements, and this is believed to facilitate further transcription factor binding events. However, the mechanisms by which many pioneer transcription factors achieve this remarkable feat remain elusive. Here we reveal that the pluripotency-associated pioneer factor OCT4 binds inaccessible chromatin to shape the chromatin accessibility, transcription factor co-binding and regulatory potential of thousands of distal regulatory elements in mouse embryonic stem cells, demonstrating that its pioneering activity is a feature of normal pluripotency, and not just reprogramming. The accessible chromatin formed at OCT4 binding sites relies on the chromatin remodelling factor BRG1, which is recruited to these sites by OCT4. The occupancy of BRG1 is then required to support OCT4/SOX2 co-binding and normal expression of the pluripotency-associated transcriptome, and this reliance on BRG1 reflects OCT4 binding dynamics during cellular reprograming and early mouse development. Together these observations reveal a distinct requirement for the chromatin remodelling factor BRG1 in shaping the pioneering activity of OCT4 and regulating the pluripotency network in embryonic stem cells.
2017-03-13 | GSE87819 | GEO
Project description:Pioneer transcription factors are able to recognise and bind their motif sequences in inaccessible or closed chromatin, and their ability to achieve this is required to establish new regulatory elements and transcriptional networks during development and cellular reprogramming. An essential feature of this pioneering activity is the transition from inaccessible chromatin to a nucleosome-depleted and accessible chromatin state typical of normal regulatory elements, and this is believed to facilitate further transcription factor binding events. However, the mechanisms by which many pioneer transcription factors achieve this remarkable feat remain elusive. Here we reveal that the pluripotency-associated pioneer factor OCT4 binds inaccessible chromatin to shape the chromatin accessibility, transcription factor co-binding and regulatory potential of thousands of distal regulatory elements in mouse embryonic stem cells, demonstrating that its pioneering activity is a feature of normal pluripotency, and not just reprogramming. The accessible chromatin formed at OCT4 binding sites relies on the chromatin remodelling factor BRG1, which is recruited to these sites by OCT4. The occupancy of BRG1 is then required to support OCT4/SOX2 co-binding and normal expression of the pluripotency-associated transcriptome, and this reliance on BRG1 reflects OCT4 binding dynamics during cellular reprograming and early mouse development. Together these observations reveal a distinct requirement for the chromatin remodelling factor BRG1 in shaping the pioneering activity of OCT4 and regulating the pluripotency network in embryonic stem cells.
2017-03-13 | GSE87820 | GEO
Project description:Microphthalmia-associated transcription factor (MITF) is the master regulator of the melanocyte lineage. To understand how MITF regulates transcription, we used tandem affinity purification and mass spectrometry to define a comprehensive MITF interactome identifying novel cofactors involved in transcription, DNA replication and repair, and chromatin organisation. We show that MITF interacts with a PBAF chromatin remodelling complex comprising BRG1 and CHD7. BRG1 is essential for melanoma cell proliferation in vitro and for normal melanocyte development in vivo. MITF and SOX10 actively recruit BRG1 to a set of MITF-associated regulatory elements (MAREs) at active enhancers. Combinations of MITF, SOX10, TFAP2A, and YY1 bind between two BRG1-occupied nucleosomes thus defining both a signature of transcription factors essential for the melanocyte lineage and a specific chromatin organisation of the regulatory elements they occupy. BRG1 also regulates the dynamics of MITF genomic occupancy. MITF-BRG1 interplay thus plays an essential role in transcription regulation in melanoma.
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Project description:We utilized MNase-seq to profile nucleosome positions in wild type (Ax2) and ChdC null cells both in growing cells and a partially developed state (loose-mound) to study changes in nucleosome positioning and occupancy during development and the impact the deletion of ChdC an ATP-dependent chromatin remodeller has on nucleosome positioning and occupancy. As a control for MNase sequence bias we also digested naked DNA with MNase.
2017-02-26 | GSE70122 | GEO
Project description:SMARCAL1 and BRG1, both classified as ATP-dependent chromatin remodeling proteins, play a role in double-strand break DNA damage response pathways. Mutations in SMARCAL1 cause Schimke Immuno-osseous Dysplasia (SIOD) while mutations in BRG1 are associated with Coffin-Siris Syndrome (CSS4). In HeLa cells, SMARCAL1 and BRG1 co-regulate the expression of ATM, ATR, and RNAi genes on doxorubicin-induced DNA damage. Both the proteins are found to be simultaneously present on the promoter of these genes. Based on these results we hypothesized that SMARCAL1 and BRG1 interact with each other forming a complex. In this paper, we validate our hypothesis and show that SMARCAL1 and BRG1 do indeed interact with each other both in the absence and presence of doxorubicin. The formation of these complexes is dependent on the ATPase activity of both SMARCAL1 and BRG1. Using deletion constructs, we show that the HARP domains of SMARCAL1 mediate interaction with BRG1 while multiple domains of BRG1 are probably important for binding to SMARCAL1. We also show that SIOD-associated mutants fail to form a complex with BRG1. Similarly, CSS4-associated mutants of BRG1 fail to interact with SMARCAL1, thus, possibly contributing to the failure of the DNA damage response pathway and pathophysiology associated with SIOD and CSS4.
| S-EPMC9243424 | biostudies-literature
Project description:The SWI/SNF complex remodels chromatin in an ATP-dependent manner through the ATPase subunits BRG1 and BRM. Chromatin remodeling alters nucleosome structure to change gene expression, however aberrant remodeling and gene expression can result in cancer. The function and localization on chromatin of the SWI/SNF complex depends on the protein makeup of the complex. Here we report the protein-protein interactions of wild-type BRG1 or mutant BRG1 in which the HSA domain has been deleted (BRG1-HSA). We demonstrate the interaction of BRG1 with most SWI/SNF complex members and a failure of a number of these members to interact with BRG1-HSA. These results demonstrate that the HSA domain of BRG1 is a critical interaction platform for the correct formation of SWI/SNF remodeling complexes.
2023-02-15 | PXD029647 | Pride
Project description:SMARCAL1 is a chromatin regulator. Biallelic mutations of SMARCAL1 cause Schimke Immunoosseous Dysplasia (SIOD), a disease with severe growth defects and premature death. Atherosclerosis and hyperlipidemia are common phenotypes among SIOD patients. However, little is known about their genesis and development. Here we show that SMARCAL1 is vital in regulating cellular lipid metabolism. Using a proteomic approach, we found that SmarcAL1 interacts with angiopoietin-like 3 (Angptl3), a key lipoprotein regulator. SmarcAL1 deficiency in cell models resulted in substantial accumulation of triglycerides (TGs) and fatty acids (FAs). SmarcAL1 KO in mice drastically increased plasma TG level. The nuclear SmarcAL1 translocates into cytoplasm, surprisingly, enriched at peroxisomes, where it interacts with Angptl3. This shuttling provides a regulatory control over cellular lipid metabolism via SmarcAL1-regulated gene expression, in response to cell growth states. Inactivation of SmarcAL1 gene reduced the expression of the genes responsible for FA metabolism, suggesting that SmarcAL1 plays a key role in regulating lipid metabolism. Indeed, the Angptl3-mediated TG partition is largely dependent on SmarcAL1 activity. This activity was further supported by two opposite SMARCAL1 single-tissue expression profiles linked to two quantitative trait loci that are differentially associated with body mass index. Thus, SMARCAL1 is crucial for cellular lipid metabolism, and ANGPTL3-regulated SMARCAL1 activities enable cells to response to cell growth states for TG storage or expenditure.
2024-01-02 | GSE221373 | GEO