Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA326876 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3720753.fastq.gz | Fastqsanger.gz | |||
| SRR3720754.fastq.gz | Fastqsanger.gz |
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Project description:Circular chromatin confirmation capture in rhabdomyosarcoma cells was performed with viewpoints at the PAX3-FOXO1 bound super enhancer upstream of MYOD1, and also at the MYOD1 promoter, to find support for looping between these two genetic elements almost 80 thousand base pairs apart.
2017-04-27 | GSE83727 | GEO
Project description:The fusion transcription factor PAX3-FOXO1 drives oncogenesis in a subset of rhabdomyosarcomas, however the mechanisms by which it remodels chromatin are unknown. We find PAX3-FOXO1 reprograms the cis-regulatory landscape by inducing super enhancers (SEs), in collaboration with master transcription factors MYOG, MYOD and MYCN. This myogenic SE circuitry is consistent across cell lines and primary tumors. Deregulation of PAX3-FOXO1 itself occurs by translocation-induced chromatin loops bringing the PAX3 promoter under the control of FOXO1 enhancers. Protein targets induced by, or bound to, PAX3-FOXO1 occupied SEs, were selectively sensitive to small molecule inhibition. PAX3-FOXO1 co-binds BRD4 at SEs, and BET bromodomains are required for PAX3-FOXO1-dependent transcription and cancer cell growth.
2017-04-27 | GSE83726 | GEO
Project description:The fusion transcription factor PAX3-FOXO1 drives oncogenesis in a subset of rhabdomyosarcomas, however the mechanisms by which it remodels chromatin are unknown. We find PAX3-FOXO1 reprograms the cis-regulatory landscape by inducing super enhancers (SEs), in collaboration with master transcription factors MYOG, MYOD and MYCN. This myogenic SE circuitry is consistent across cell lines and primary tumors. Deregulation of PAX3-FOXO1 itself occurs by translocation-induced chromatin loops bringing the PAX3 promoter under the control of FOXO1 enhancers. Protein targets induced by, or bound to, PAX3-FOXO1 occupied SEs, were selectively sensitive to small molecule inhibition. PAX3-FOXO1 co-binds BRD4 at SEs, and BET bromodomains are required for PAX3-FOXO1-dependent transcription and cancer cell growth.
2017-04-27 | GSE83725 | GEO
Project description:The fusion transcription factor PAX3-FOXO1 drives oncogenesis in a subset of rhabdomyosarcomas, however the mechanisms by which it remodels chromatin are unknown. We find PAX3-FOXO1 reprograms the cis-regulatory landscape by inducing super enhancers (SEs), in collaboration with master transcription factors MYOG, MYOD and MYCN. This myogenic SE circuitry is consistent across cell lines and primary tumors. Deregulation of PAX3-FOXO1 itself occurs by translocation-induced chromatin loops bringing the PAX3 promoter under the control of FOXO1 enhancers. Protein targets induced by, or bound to, PAX3-FOXO1 occupied SEs, were selectively sensitive to small molecule inhibition. PAX3-FOXO1 co-binds BRD4 at SEs, and BET bromodomains are required for PAX3-FOXO1-dependent transcription and cancer cell growth.
2017-04-27 | GSE83724 | GEO
Project description:Results: Using a combination of 4C-seq datasets, we were able to model the three-dimensional organisation of the translocated chromosome in a PAX3:FOXO1 fusion-positive alveolar rhabdomyosarcoma cell line. We show that PAX3 and FOXO1 regulatory landscapes fuse into a novel TAD, allowing the PAX3 promoter to interact ectopically with FOXO1 sequences with potential enhancer function. The borders of this novel TAD correspond to the original 5'- and 3'- borders of the PAX3 and FOXO1 TADs, respectively, suggesting that TAD organisation precedes the formation of regulatory long-range interactions. Conclusions: Our results suggest that the chromosomal translocation that leads to ARMS development generates a novel TAD that favours ectopic PAX3:FOXO1 oncogene activation in non-PAX3 territories, which may be an essential step in the tumorigenic process, as expression in a particular cell type, the often elusive cell-of-origin, may be required for disease development.
2017-04-17 | GSE69439 | GEO
Project description:The viewpoints used in the 4C-seq data were either the EVI1 promoter or the MYC super-enhancer
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Project description:Super-enhancers may regulate target genes through chromatin looping. We connected super-enhancers in the K562 chronic myelogenous leukemia cell line with chromatin interactions identified from Chromatin Interaction Analysis with Paired-End Tag (ChIA-PET) data. Gene expression at proximal elements that are connected with distal super-enhancers showed significantly higher cell-type specificity than at proximal elements connected with other elements or not involved in interaction. 4C and Episwitch analysis of chromatin interactions showed that certain chromatin interactions are cell-specific, but others are more general. While super-enhancers upstream of c-MYC at the MYC-335 element can be found in other cancers, only super-enhancers downstream of c-MYC can be found in K562. 4C analysis of the c-MYC promoter revealed no chromatin interactions that are directed upstream of c-MYC, but only downstream of c-MYC, in the PVT1 long non-coding RNA gene. Cell-specific usage of super-enhancers could explain why the MYC-335 element that is associated with many solid cancers such as colorectal cancer and breast cancer, but not with leukemia. Surprisingly, we found that a chromatin interaction between c-MYC and a c-MYC super-enhancer is lost in chronic myelogenous leukemia patient blood as compared with blood from individuals without the disease through Oxford Biodynamicsâ?? Episwitch analysis. These results provide evidence for fine-tuning of expression patterns, such as cell-specific regulation of target genes by distal super-enhancers through chromatin interactions and an association between chromatin interactions and disease, and highlight that super-enhancers are more complex than previously described. Examination of several chromatin interactions involving super-enhancers using 4C-Seq and Episwitch (TM)
2017-05-01 | E-GEOD-77125 | biostudies-arrayexpress
Project description:Studying the dynamics of three-dimensional (3D) chromatin structure is essential to the understanding of biological processes in the nucleus. Integrative analysis of multi-omics data in recent publications have provided comprehensive and multilevel insight into 3D genome organization emphasizing its role for transcriptional regulation. While enhancers are regulatory elements that play a central role in the spatiotemporal control of gene expression, chromatin looping has been broadly accepted as a means for enhancer-promoter interactions yieldingcell-type-specific gene expression signatures. On the other hand, G-quadruplexes (G4s) are non-canonical DNA secondary structures that are enriched at promoters and related to increased gene expression, both. A role for G4s in promoter-distal regulatory elements, such as super-enhancers (SE), as well as in 3D genome organization and chromatin looping mediating long-range enhancer-promoter interactions has, however, remained elusive. Here we show that mature microRNA 9 (miR-9) is enriched at promoters and SE of genes that are inducible by tissue growth factor beta 1 (TGFB1) signaling. Further, we find that nuclear miR-9 is required for chromatin features related to increased transcriptional activity, such as broad domains of the euchromatin histone mark H3K4me3 (histone 3 tri-methylated lysine 4) and G4s. Moreover, we show that nuclear miR-9 is required for promoter-super-enhancer looping. Our study places a nuclear microRNA in the same structural and functional context with G4s and promoter-enhancer interactions during 3D genome organization and transcriptional activation induced by TGFB1 signaling, a critical regulator of proliferation programs in cancer and fibrosis.
2024-07-30 | MSV000095480 | MassIVE
Project description:To determine whether a TP63/KLF5-regulated super-enhancer region can impact SREBF1 transcription, circularized chromosome conformation capture (4C) assays were performed. 4C assays identified complex, extensive interactions between the SREBF1 promoter and the super-enhancer region Moreover, these DNA-DNA contacts were strictly confined within the super-enhancer region, highlighting the specificity of chromatin interactions
2021-06-26 | GSE178923 | GEO
Project description:Chromatin looping allows enhancer-bound regulatory factors to influence transcription. Large domains, referred to as Topologically Associated Domains (TADs), participate in genome organization but the mechanisms underlining interactions within TADs, that actually control gene expression, are largely unknown. Here we report that activation of embryonic myogenesis is associated with establishment of long-range chromatin interactions centered on Pax3-bound loci. Using mass spectrometry and genomic studies, we identified the ubiquitously expressed LIM-domain binding protein 1 (Ldb1) as the mediator of looping interactions at a subset of Pax3 binding sites. Ldb1 is recruited to Pax3-bound elements independently of CTCF-Cohesin, and is necessary for efficient deposition of H3K4me1 at these sites and chromatin looping. When Ldb1 is deleted in Pax3-expressing cells in vivo, specification of migratory myogenic progenitors is severely impaired. These results highlight Ldb1 requirement for Pax3 myogenic activity and demonstrate how a transcription factor promotes formation of sub-TAD interactions associated with lineage specification.
2019-04-16 | GSE126362 | GEO