ChIP-Seq of Pax7 and Pax3 in myoblasts
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE25064 | GEO | 2012/05/22
SECONDARY ACCESSION(S): PRJNA142729
REPOSITORIES: GEO
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Project description:Examination of binding locations of Pax3 and Pax7 in primary myoblasts UCSC track hub available at: http://www.ogic.ca/projects/Soleimani_2012_Pax7_hub/hub.txt For details on viewing the track hub in the UCSC Genome Browser: http://altair.dartmouth.edu/ucsc/goldenPath/help/hgTrackHubHelp.html#View 3 Samples (Control, Pax7 ChIP, Pax3 ChIP)
2012-05-22 | E-GEOD-25064 | biostudies-arrayexpress
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Project description:Hallmarks of the alveolar subclass of Rhabdomyosarcoma are chromosomal translocations that generate PAX3-FOXO1 or PAX7-FOXO1 chimeric transcription factors. Both PAX-FOXO1s drive related cell transformation in animal models, yet the two mutations are associated with distinct pathological manifestations in patients. To evaluate the mechanisms underlying these differences, we generated isogenic fibroblast lines expressing either PAX-FOXO1 paralog. Mapping their genome recruitment using CUT&Tag revealed that the two chimeric proteins have distinct DNA binding preferences. Furthermore, PAX7-FOXO1 causes stronger de novo transactivation of its bound regions than PAX3-FOXO1, resulting in greater transcriptomic dynamics involving genes regulating cell shape and cycle. Consistently, PAX3-FOXO1 accentuates fibroblast cellular traits associated with contractility and surface adhesion and limits entry to M phase. Instead, PAX7-FOXO1 pushes cells to adopt an amoeboid-like shape, reduce S phase entry and provokes more genome instabilities. Altogether, our results demonstrate that PAX7-FOXO1 has a greater chromatin remodelling and transactivating abilities and is more deleterious to cells than PAX3-FOXO1. Altogether our results argue that the diversity in rhabdomyosarcoma manifestation stems, in part, from the diverging transcriptional activity of PAX3-FOXO1 and PAX7-FOXO1. Furthermore, PAX7-FOXO1 pronounced deleterious effects provides an explanation for the low frequency of the translocation generating this factor in Rhabdomyosarcoma patients.
2021-08-15 | GSE180919 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE25064: ChIP-Seq of Pax7 and Pax3 in myoblasts GSE32266: Mouse Myoblast Pax3, Pax7 overexpression and control Refer to individual Series
2012-05-22 | E-GEOD-25092 | biostudies-arrayexpress
Project description:Pax7 is a paired box transcription factor that is central to skeletal muscle satellite cell function Microarrays were used to examine gene expression after primary murine satellite cell-derived myoblasts were retrovirally infected with constructs encoding Pax7, PAX7-FOXO1A, dominant negative Pax7-ERD and retroviral control.
2017-02-01 | GSE77478 | GEO
Project description:Divergent transcriptional and transforming properties of PAX3-FOXO1 and PAX7-FOXO1 paralogs
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Project description:Exposure to environmental teratogenic pollutant leads to severe birth defects. However, the biological events underlying these developmental abnormalities remain undefined. Here we report a molecular link between an environmental stress response pathway and key developmental genes during craniofacial development. In our study, we focused on the development of the facial prominences at E11.5. To do so, we compared the transcriptomes of mutant embryos (*Pax3Pax3-ERD/GFP *called DM in the microarray samples) to the one of control embryos (*Pax3GFP/+ *called GFP in the sample names). These are knock-in genetic models described in Bajard et al., 2006 and Relaix et al., 2005. In both of them a cassette coding for the GFP is replacing one allele of the Pax3 gene. The Pax3-ERD allele is a conditional one that drives the expression of the dominant negative form of Pax3 (Pax3-ERD) composed of the Pax3 DNA binding domain fused to the engrailed repressor domain (ERD) upon activation of a Cre recombinase. In this study, the Cre was driven by the zygote specific PGK enhancer. Strikingly, mutant mice with impaired Pax3/7 function display severe craniofacial defects. We show these are associated with an up-regulation of the signaling pathway mediated by the Aryl hydrocarbon Receptor (AhR), the receptor to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), revealing a genetic interaction between Pax3 and AhR signaling. Activation of AhR signaling in Pax3-deficient embryos drives facial mesenchymal cells out of the cell cycle through the up-regulation of p21 expression. Accordingly, inhibiting AhR activity rescues the cycling status of these cells and the facial closure of Pax3/7 mutants. Together, our findings demonstrate that the regulation of AhR signaling by Pax3/7 is required to protect against TCDD/AhR-mediated teratogenesis during craniofacial development.
2015-04-06 | E-MTAB-3238 | biostudies-arrayexpress
Project description:Sequencing files, and processed data correspond to Figure 3 of Regenerating Human Skeletal Muscle Forms an Emerging Niche In Vivo to Support PAX7 cells. Data contains single nucleus RNA seq from Pax7 ablated mdx-NSG mice, control mdx-NSG mice, with or without an injury. These mice offer superior engraftment by human skeletal muscle stem and progenitor cells. Pax7 ablation model enables evaluation of human stem cell niche formation in the absence of mouse Pax7 cell competition. Included in this dataset is everything required to run independent analysis. We have included raw Fastq files and processed files that are ready to be uploaded into Loupe Browser or R-Studio/Seurat V3. To summarize Cloupe Files can be uploaded to Loupe Browers and the BC_Matrix.H5 files can be uploaded directly to R. Furthermore, the RDS files are processed R-program files that can be immediately uploaded into R for analysis. We have included an example R script for users to follow and a few PDFs of excepted UMAPs using all combined files at PCA 35.
2023-09-22 | GSE241368 | GEO
Project description:PAX3-FOXO1 is a fusion transcription factor that is the main driver of tumorigenesis leading to the development of alveolar rhabdomyosarcoma (aRMS). Since aRMS cells are addicted to PAX3-FOXO1 activity, the fusion protein also represents a major target for therapeutic interference, which is however challenging as transcription factors usually cannot be inhibited directly by small molecules. Hence, characterization of the biology of PAX3-FOXO1 might lead to the discovery of new possibilities for an indirect inhibition of its activity. Here, our goal was to characterize the proteomic neighborhood of PAX3-FOXO1 and to find candidates potentially affecting its activity and tumor cell viability. Towards this aim, we expressed BirA fused versions of PAX3-FOXO1 (N- and C-terminal) in HEK293T cells under presence of biotin. In the control setup, we expressed the BirA enzyme alone. After Streptavidin purification of biotinylated proteins, we performed mass spectrometry and quantified relative abundances compared to control conditions. This enabled us to determine PAX3-FOXO1 proximal proteins, which we investigated further in orthogonal endogenous systems.
2021-09-16 | PXD022187 | Pride