Chip-chip from Mouse E11.5 distal limb tissue cells for Gabpa, Ets1, Elf1, Etv4, Etv5 antibody
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE33997 | GEO | 2012/02/01
SECONDARY ACCESSION(S): PRJNA150569
REPOSITORIES: GEO
Similar Datasets
Project description:Two different groups of Ets transcription factors differentially act directly at the ZRS to define the spatial expression of Shh in the limb. Chromatin immunoprecipitation (ChIP) of Gabpa, Ets1, Etv4, Etv5 and Elf1 and by ChIP-on-chip analysis demonstrated that with the exception of Elf1 all bind directly to the Shh limb enhancer, the ZRS. Array design includes 2 biological replicates for Gabpa and Elf1, and two biological replicates and one dye swap replicate for Ets1, Etv4 and Etv5 samples.
2012-02-01 | E-GEOD-33997 | biostudies-arrayexpress
Project description:ChIP profiling of transcription factor Etv4 (Pea3) Gabpa, Histone deacetylase HDAC2, Ep300 and Histone tails H3K4me1 and H3K27ac in E11.5 limb derived cell line (14Fp ) across the ZRS and a selection of limb development genes
2018-01-01 | GSE104207 | GEO
Project description:Limb-specific expression of Shh is regulated by the long-range (~one megabasepair distant) ZRS enhancer. In the mouse, murine limb bud restricted spatiotemporal expression of Shh occurs from ~E10 until E11.5 at the distal posterior margin is essential for the correct formation of the autopod. Here, we have analyzed the higher-order chromatin conformation of Shh in expressing and non-expressing tissues, both by fluorescence in situ hybridization (FISH) and by chromosome conformation capture (5C). Conventional and super-resolution light microscopy identified significantly elevated frequences of Shh/ZRS co-localization only in the Shh expressing regions of the limb bud consistent with the formation of an enhancer-promoter loop. However, Shh-ZRS spatial distances were consistently shorter than intervening distances to a neural enhancer in all tissues and developmental stages analyzed – regardless of Shh expression. 5C also identified a topologically associating domain (TAD) over the Shh-ZRS genomic region and enriched interactions between Shh and ZRS, but in the head, body and limb buds of E11.5 embryos, so also not linked to Shh expression. We show that gene-enhancer (Shh/ZRS) co-localization correlates with the spatiotemporal domain of limb bud-specific Shh expression, but that close Shh/ZRS proximity in the nucleus occurs regardless of whether the gene or enhancer is active. We suggest that this constrained chromatin configuration optimises the opportunity for the active enhancer to locate and instigate Shh expression.
2016-05-03 | GSE79947 | GEO
Project description:Acheiropodia, congenital limb truncation, is associated with homozygous deletions in the LMBR1 gene around ZRS, an enhancer regulating SHH during limb development. How these deletions leads to this phenotype is unknown. Using whole-genome sequencing, we fine-mapped the acheiropodia-associated region to 12 kb and show that it does not function as an enhancer. CTCF and RAD21 ChIP-seq together with 4C-seq and DNA FISH identify three CTCF sites within the acheiropodia-deleted region that mediate the interaction between the ZRS and the SHH promoter. This interaction is substituted with other CTCF sites centromeric to the ZRS in the disease state. Mouse knockouts of the orthologous 12 kb sequence have no apparent abnormalities, showcasing the challenges in modelling CTCF alterations in animal models due to inherent motif differences between species. Our results show that alterations in CTCF motifs can lead to a Mendelian condition due to altered enhancer-promoter interactions.
2020-07-30 | GSE155324 | GEO
Project description:The goal of this study was to analyze the DNA binding landscape of ELF1 in A549 cells. We found that ELF1 mostly binds promoters of genes, close to transcription start sites. We used the promoter-bound genes from our ChIP-seq data and intersected it with differentially expressed genes upon ELF1 overexpression in A549 cells to identify a set of ELF1 regulated target genes.
2019-10-24 | GSE122203 | GEO
Project description:Expression of Shh in the limb is dependent on a distant enhancer located 850kb away from the gene promoter. We performed chromatin conformation capture (4C-Seq) analysis of the Shh locus in E11.5 mouse limbs so as to better understand the relationship between this regulatory interaction and the structural organisation of the locus. The experiments were performed on wild-type animals as well as on animals carrying an engineered chromosomal inversion (INV(6-C2) (INV6)) . The different viewpoints used (Shh, ZRS, Nom1, Rbm33, Rnf32) enable to characterize the 3D organisation of the locus in the different contexts. The inversion INV6 disrupts the normal topological organisation of the Shh locus in a compact 3D-domain and prevents the physical and regulatory interaction between Shh and its limb enhancer, even though the genomic distance separating the two elements is reduced compared to WT.
2017-01-12 | E-MTAB-4980 | biostudies-arrayexpress
Project description:Chip-chip from Mouse E11.5 distal limb tissue cells for Gabpa, Ets1, Elf1, Etv4, Etv5 antibody
| PRJNA150569 | ENA
Project description:During embryogenesis, enhancer-promoter interactions control gene transcriptional activation. These interactions can be tissue-specific or tissue-invariant and occur mostly within larger insulated regulatory domains called Topologically Associating Domains (TADs). Boundary elements, which delineate the extent of TADs, frequently interact with each other and have been associated with constitutive transcription and CTCF/Cohesin binding. In this work, we set out to investigate the regulatory role of a tissue-invariant, preformed interaction between two boundaries that involve the Shh gene and its unique limb enhancer, the ZRS, located one megabase away. Using CRISPR/Cas9 we specifically perturb CTCF binding sites or constitutive transcription at the ZRS-containing boundary, without altering the enhancer sequence. Using capture-HiC (cHiC) we show that both types of perturbation result in altered preformed chromatin interactions and lead to a reduction of Shh expression in developing limb buds. Finally, we demonstrate that the disruption of the chromatin structure in combination with a hypomorphic ZRS allele results in a dramatic Shh loss- of- function and digit agenesis. We thus propose that preformed chromatin structures can ensure stable enhancer promoter communication during development and robustness of gene transcriptional activation.
2019-05-13 | GSE123387 | GEO
Project description:During embryogenesis, enhancer-promoter interactions control gene transcriptional activation. These interactions can be tissue-specific or tissue-invariant and occur mostly within larger insulated regulatory domains called Topologically Associating Domains (TADs). Boundary elements, which delineate the extent of TADs, frequently interact with each other and have been associated with constitutive transcription and CTCF/Cohesin binding. In this work, we set out to investigate the regulatory role of a tissue-invariant, preformed interaction between two boundaries that involve the Shh gene and its unique limb enhancer, the ZRS, located one megabase away. Using CRISPR/Cas9 we specifically perturb CTCF binding sites or constitutive transcription at the ZRS-containing boundary, without altering the enhancer sequence. Using capture-HiC (cHiC) we show that both types of perturbation result in altered preformed chromatin interactions and lead to a reduction of Shh expression in developing limb buds. Finally, we demonstrate that the disruption of the chromatin structure in combination with a hypomorphic ZRS allele results in a dramatic Shh loss- of- function and digit agenesis. We thus propose that preformed chromatin structures can ensure stable enhancer promoter communication during development and robustness of gene transcriptional activation.
2019-05-13 | GSE123386 | GEO
Project description:During embryogenesis, enhancer-promoter interactions control gene transcriptional activation. These interactions can be tissue-specific or tissue-invariant and occur mostly within larger insulated regulatory domains called Topologically Associating Domains (TADs). Boundary elements, which delineate the extent of TADs, frequently interact with each other and have been associated with constitutive transcription and CTCF/Cohesin binding. In this work, we set out to investigate the regulatory role of a tissue-invariant, preformed interaction between two boundaries that involve the Shh gene and its unique limb enhancer, the ZRS, located one megabase away. Using CRISPR/Cas9 we specifically perturb CTCF binding sites or constitutive transcription at the ZRS-containing boundary, without altering the enhancer sequence. Using capture-HiC (cHiC) we show that both types of perturbation result in altered preformed chromatin interactions and lead to a reduction of Shh expression in developing limb buds. Finally, we demonstrate that the disruption of the chromatin structure in combination with a hypomorphic ZRS allele results in a dramatic Shh loss- of- function and digit agenesis. We thus propose that preformed chromatin structures can ensure stable enhancer promoter communication during development and robustness of gene transcriptional activation.
2019-05-13 | GSE123384 | GEO