Mapping BRD1 and HBO1 genomic binding in BRCA1 mutant cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1021065 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26176727_1.fastq.gz | Fastqsanger.gz | |||
| SRR26176727_2.fastq.gz | Fastqsanger.gz | |||
| SRR26176728_1.fastq.gz | Fastqsanger.gz | |||
| SRR26176728_2.fastq.gz | Fastqsanger.gz | |||
| SRR26176729_1.fastq.gz | Fastqsanger.gz |
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Project description:The BRCA1 tumor suppressor has many functions in DNA damage repair, DNA replication, and beyond. Loss of any of these functions can lead to breast and ovarian carcinogenesis and also therapeutic sensitivity. In this study, we have discovered a novel role for BRCA1 in controlling replication initiation by regulating the bromodomain-protein BRD1 and the histone acetyltransferase HBO1. Specifically, we show that BRCA1 regulates localization of the BRD1-HBO1 complex to replication origins where the complex normally acetylates histone H3 on lysine 14. We performed chromatin-immunoprecipitation seqeuncing (ChIP-seq) for BRD1 and HBO1 in a BRCA1 mutant line (UWB1.289) and demonstrate that BRD1 and HBO1 co-occupy ORC2 binding sites and replication origins.
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Project description:We identified chromatin binding sites for two isforms of BRD1 (BRD1-S and BRD1-L) using ChIP-seq.
2015-10-29 | GSE62811 | GEO
Project description:We identified protein-protein interactions and chromatin binding sites for two isforms of BRD1 (BRD1-S and BRD1-L) using Co-IP MS/MS and ChIP-seq. BRD1 isoforms were cloned, epitope-tagged (pcDNA 6 V5-His6, Lifetechnologies) and stably expressed in HEK293T cells. Chromatin immunoprecipitations were performed using anti V5-antibody conjugated agarose beads (Sigma-Aldrich) and anti HA antibody conjugated agarose beads (Sigma-Aldrich) as controls
2015-10-29 | E-GEOD-62811 | biostudies-arrayexpress
Project description:Background: The bromodomain containing 1 (BRD1) gene has been implicated with transcriptional regulation, brain development and susceptibility to schizophrenia and bipolar disorder. Results: To advance the understanding of BRD1 and its role in mental disorders, we characterized the protein and chromatin interactions of the BRD1 isoforms, BRD1-S and BRD1-L, by a series of investigations and integration of functional molecular data with human genetic data. We present several novel protein interactions of BRD1, including proteins previously implicated with mental disorders. By BRD1-S and BRD1-L chromatin immunoprecipitation followed by next generation sequencing we identified binding to promoter regions of 1540 and 823 genes, respectively, and showed correlation between BRD1-S and BRD1-L binding and regulation of gene expression. The identified BRD1 interaction network was found to be predominantly co-expressed with BRD1 mRNA in human brain and enriched for pathways involved in gene expression and brain function. By interrogation of large data sets from genome-wide association studies, we further demonstrate that the BRD1 interaction network is enriched for schizophrenia risk. Conclusion: Our results show that BRD1 interacts with chromatin remodeling proteins, e.g. PBRM1, as well as histone modifiers, e.g. MYST2 and SUV420H1. We find that BRD1 primarily binds in close proximity to transcription start sites and regulates expression of numerous genes, many of which are involved with brain development and susceptibility to mental disorders. Our findings indicate that BRD1 acts as a regulatory hub in a comprehensive schizophrenia risk network which plays a role in many brain regions throughout life, implicating e.g.striatum, hippocampus, and amygdala at mid fetal stages. 9 expression arrays performed in HEK293T cells
2016-03-16 | E-GEOD-79255 | biostudies-arrayexpress
Project description:Background: The bromodomain containing 1 (BRD1) gene has been implicated with transcriptional regulation, brain development and susceptibility to schizophrenia and bipolar disorder. Results: To advance the understanding of BRD1 and its role in mental disorders, we characterized the protein and chromatin interactions of the BRD1 isoforms, BRD1-S and BRD1-L, by a series of investigations and integration of functional molecular data with human genetic data. We present several novel protein interactions of BRD1, including proteins previously implicated with mental disorders. By BRD1-S and BRD1-L chromatin immunoprecipitation followed by next generation sequencing we identified binding to promoter regions of 1540 and 823 genes, respectively, and showed correlation between BRD1-S and BRD1-L binding and regulation of gene expression. The identified BRD1 interaction network was found to be predominantly co-expressed with BRD1 mRNA in human brain and enriched for pathways involved in gene expression and brain function. By interrogation of large data sets from genome-wide association studies, we further demonstrate that the BRD1 interaction network is enriched for schizophrenia risk. Conclusion: Our results show that BRD1 interacts with chromatin remodeling proteins, e.g. PBRM1, as well as histone modifiers, e.g. MYST2 and SUV420H1. We find that BRD1 primarily binds in close proximity to transcription start sites and regulates expression of numerous genes, many of which are involved with brain development and susceptibility to mental disorders. Our findings indicate that BRD1 acts as a regulatory hub in a comprehensive schizophrenia risk network which plays a role in many brain regions throughout life, implicating e.g.striatum, hippocampus, and amygdala at mid fetal stages.
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Project description:We used ChIP-seq technology in order to map chromatin binding sites of the HBO1 MYST complex in the RKO cell line. We obtained a significant enrichment of the HBO1 signal right after TSS regions of genes and also In the proximal promoter region, with no signal on TSS. This enrichment also correlates with gene expression level. HBO1 signal in RKO cell line.
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Project description:We find that 499 genes are up-regulated and 457 are down-regulated in response to over-expression of JADE1, while 397 genes are up-regulated and 385 are down-regulated after HBO1 knock-down. For each condition - HBO1 siRNA treatment or JADE1 over-expression - two biological replicates were analyzed in duplicate.
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Project description:Epigenomic dysregulation is widespread in cancer. However, the specific epigenomic regulators and the processes they control to drive cancer phenotypes are poorly understood. We employed a novel, scalable and high-throughput in vivo method to perform iterative functional screens of >250 epigenomic regulators within autochthonous oncogenic KRAS-driven lung tumors. We identified many previously unappreciated epigenomic tumor-suppressor and tumor-dependency genes. We show that a specific HBO1 complex and MLL1 complex are robust tumor suppressors in lung cancer. Histone modifications generated by HBO1 complex are frequently diminshed in human lung adenocarcinomas and is associated with worse clinical features. HBO1 and MLL1 complexes co-occupy shared genomic regions, impacting chromatin accessibility, expression of canonical tumor suppressor genes and lineage fidelity. The HBO1 complex is epistatic with the MLL1 complex and other tumor suppressor genes in lung adenocarcinoma development. Collectively, these results uncover HBO1 and MLL1 complexes as critical functional modules restraining lung adenocarcinoma development and provide a in vivo phenotypic roadmap of epigenomic regulators in lung tumorigenesis.
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Project description:Epigenomic dysregulation is widespread in cancer. However, the specific epigenomic regulators and the processes they control to drive cancer phenotypes are poorly understood. We employed a novel, scalable and high-throughput in vivo method to perform iterative functional screens of >250 epigenomic regulators within autochthonous oncogenic KRAS-driven lung tumors. We identified many previously unappreciated epigenomic tumor-suppressor and tumor-dependency genes. We show that a specific HBO1 complex and MLL1 complex are robust tumor suppressors in lung cancer. Histone modifications generated by HBO1 complex are frequently diminshed in human lung adenocarcinomas and is associated with worse clinical features. HBO1 and MLL1 complexes co-occupy shared genomic regions, impacting chromatin accessibility, expression of canonical tumor suppressor genes and lineage fidelity. The HBO1 complex is epistatic with the MLL1 complex and other tumor suppressor genes in lung adenocarcinoma development. Collectively, these results uncover HBO1 and MLL1 complexes as critical functional modules restraining lung adenocarcinoma development and provide a in vivo phenotypic roadmap of epigenomic regulators in lung tumorigenesis.
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Project description:Epigenomic dysregulation is widespread in cancer. However, the specific epigenomic regulators and the processes they control to drive cancer phenotypes are poorly understood. We employed a novel, scalable and high-throughput in vivo method to perform iterative functional screens of >250 epigenomic regulators within autochthonous oncogenic KRAS-driven lung tumors. We identified many previously unappreciated epigenomic tumor-suppressor and tumor-dependency genes. We show that a specific HBO1 complex and MLL1 complex are robust tumor suppressors in lung cancer. Histone modifications generated by HBO1 complex are frequently diminshed in human lung adenocarcinomas and is associated with worse clinical features. HBO1 and MLL1 complexes co-occupy shared genomic regions, impacting chromatin accessibility, expression of canonical tumor suppressor genes and lineage fidelity. The HBO1 complex is epistatic with the MLL1 complex and other tumor suppressor genes in lung adenocarcinoma development. Collectively, these results uncover HBO1 and MLL1 complexes as critical functional modules restraining lung adenocarcinoma development and provide a in vivo phenotypic roadmap of epigenomic regulators in lung tumorigenesis.
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