Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA128699 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We report the comparative investigation of genome-wide chromatin state maps, transcription factor (TF) occupancy, and gene expression profiles from developing red cell precursors at two developmental stages. Contrasting the similarities and differences between fetal and adult erythropoiesis provides important insights into the erythroid gene expression programs and gene regulatory networks. Specifically, comparative analyses of human erythropoiesis identify developmental stage-specific enhancers as primary determinants of stage-specific gene expression programs. We find that master regulators, such as GATA1 and TAL1, cooperatively act within active enhancers but have little predictive value for stage-specific enhancer activity. Instead, a set of stage-specific co-regulators collaborates with master regulators and contributes to differential gene expression. We further identify and validate IRF2, IRF6, and MYB as effectors of adult-stage expression program. Thus, the combinatorial assembly of master regulators and transcriptional co-regulators at developmental stage-specific enhancers controls gene expression programs and temporal regulation of transcriptional networks in a mammalian genome. Examination of various histone modifications and transcription factor occupancy by ChIP-seq in fetal and adult proerythroblasts.
2012-10-05 | E-GEOD-36985 | biostudies-arrayexpress
Project description:Genome-wide Myb chromatin occupancy in murine myeloid progenitor cells
| PRJNA128833 | ENA
Project description:We report genome-wide pattern of Myb chromatin occupancy in vivo. We used ERMYB, a myeloid progenitor cell line derived by transformation of primary cells by ER-Myb fusion protein, as our model system. In these cells, activation of the ER-Myb fusion protein by estrogen is required to maintain a proliferative progenitor-like phenotype. We performed ChIP-seq with biological duplicate samples from ERMYB cells with Myb either “on” or “off” (i.e. + or - ?-E2 for 6 hr). By comparing enrichment signals between Myb-on, Myb-off and isotype control samples, we identified 7,646 high-confidence Myb binding regions, which can be assigned to 4,892 annotated genes according to their distances to the nearest transcriptional start sites. Examination of Myb chromatin occupany in myeloid cells transformed by a switchable form of Myb
2011-02-23 | E-GEOD-22095 | biostudies-arrayexpress
Project description:Pancreatic cancer is an aggressive malignancy, characterized by extensive desmoplasia and a hypoxic tumor microenvironment that contributes to therapy resistance. MYB, a proto-oncogene encoding a transcription factor, plays a crucial role in pancreatic tumor growth, metastasis, and desmoplasia. Recently, we also revealed a role of MYB in hypoxic survival of pancreatic cancer by promoting metabolic reprogramming through interaction with HIF1α, modulating its expression and influencing its binding to glycolytic gene promoters. In this study, we examined the impact of hypoxia on the genome-wide occupancy of MYB by performing chromatin immunoprecipitation sequencing (ChIP-seq) analysis. We also used HIF1A knockout cells to investigate the role of HIF1α in altered genomic occupancy of MYB. In addition, we examined the genomic distribution of HIF1α in presence and absence of MYB and the impact of their crosstalk on transcriptional reprogramming and associated signaling alterations by RNA-seq and pathway analyses. Our findings show that hypoxia induces significant changes in MYB’s genomic distribution, partially dependent on HIF1α, and that MYB facilitates HIF1α binding to specific gene promoters. We also identify a subset of hypoxia-induced genes co-regulated by MYB and HIF1α, involved in oncogenic signaling pathways critical for hypoxic adaptation. These results highlight the reciprocal crosstalk between MYB and HIF1α, providing novel mechanistic insights into pancreatic cancer adaptation under hypoxia and suggesting MYB as a potential therapeutic target.
2025-07-17 | GSE292665 | GEO
Project description:Pancreatic cancer is an aggressive malignancy, characterized by extensive desmoplasia and a hypoxic tumor microenvironment that contributes to therapy resistance. MYB, a proto-oncogene encoding a transcription factor, plays a crucial role in pancreatic tumor growth, metastasis, and desmoplasia. Recently, we also revealed a role of MYB in hypoxic survival of pancreatic cancer by promoting metabolic reprogramming through interaction with HIF1α, modulating its expression and influencing its binding to glycolytic gene promoters. In this study, we examined the impact of hypoxia on the genome-wide occupancy of MYB by performing chromatin immunoprecipitation sequencing (ChIP-seq) analysis. We also used HIF1A knockout cells to investigate the role of HIF1α in altered genomic occupancy of MYB. In addition, we examined the genomic distribution of HIF1α in presence and absence of MYB and the impact of their crosstalk on transcriptional reprogramming and associated signaling alterations by RNA-seq and pathway analyses. Our findings show that hypoxia induces significant changes in MYB’s genomic distribution, partially dependent on HIF1α, and that MYB facilitates HIF1α binding to specific gene promoters. We also identify a subset of hypoxia-induced genes co-regulated by MYB and HIF1α, involved in oncogenic signaling pathways critical for hypoxic adaptation. These results highlight the reciprocal crosstalk between MYB and HIF1α, providing novel mechanistic insights into pancreatic cancer adaptation under hypoxia and suggesting MYB as a potential therapeutic target.
2025-07-17 | GSE292666 | GEO
Project description:We report genome-wide pattern of Myb chromatin occupancy in vivo. We used ERMYB, a myeloid progenitor cell line derived by transformation of primary cells by ER-Myb fusion protein, as our model system. In these cells, activation of the ER-Myb fusion protein by estrogen is required to maintain a proliferative progenitor-like phenotype. We performed ChIP-seq with biological duplicate samples from ERMYB cells with Myb either “on” or “off” (i.e. + or - β-E2 for 6 hr). By comparing enrichment signals between Myb-on, Myb-off and isotype control samples, we identified 7,646 high-confidence Myb binding regions, which can be assigned to 4,892 annotated genes according to their distances to the nearest transcriptional start sites.
2011-02-23 | GSE22095 | GEO
Project description:We report the comparative investigation of genome-wide chromatin state maps, transcription factor (TF) occupancy, and gene expression profiles from developing red cell precursors at two developmental stages. Contrasting the similarities and differences between fetal and adult erythropoiesis provides important insights into the erythroid gene expression programs and gene regulatory networks. Specifically, comparative analyses of human erythropoiesis identify developmental stage-specific enhancers as primary determinants of stage-specific gene expression programs. We find that master regulators, such as GATA1 and TAL1, cooperatively act within active enhancers but have little predictive value for stage-specific enhancer activity. Instead, a set of stage-specific co-regulators collaborates with master regulators and contributes to differential gene expression. We further identify and validate IRF2, IRF6, and MYB as effectors of adult-stage expression program. Thus, the combinatorial assembly of master regulators and transcriptional co-regulators at developmental stage-specific enhancers controls gene expression programs and temporal regulation of transcriptional networks in a mammalian genome.
2012-10-05 | GSE36985 | GEO
Project description:The Myb proto-oncogene encodes the transcription factor c-MYB, which is critical for the proliferation and differentiation of hematopoietic stem and progenitor cells. Distant enhancers of Myb expression have been characterized but the regulation of Myb during hematopoiesis is still incompletely understood. Here we identified a novel nuclear Myb enhancer long intergenic non-coding RNA (Myrlin) that originates from the -81 kb murine Myb enhancer within the Myb ─ Hbs1l intergenic region. Myrlin and Myb are coordinately regulated in a developmental stage-specific fashion during maturation of erythroid progenitors and upon differentiation of MEL cells. CRISPR/Cas9 genome editing of the Myrlin transcription start site at the -81kb enhancer reduced both Myrlin and Myb expression. The deletion of Myrlin TSS reduces the occupancy of LDB1, which mediates chromatin looping, and compromises long-range contacts between the Myb promoter and enhancer and RNA Pol II occupancy decreases across the Myb locus. In contrast, silencing of Myrlin using CRISPRi similarly reduced both Myrlin and Myb expression but left the Myb enhancer hub undisturbed, separating chromatin looping from transcription activation of Myb. In unedited cells, we found that Myrlin interacts with MLL1 complex, a transcriptional coactivator that plays an essential role in regulating gene expression during hematopoiesis. Myrlin CRISPRi compromised MLL1 occupancy in the Myb locus and decreased CDK9 and RNA Pol II binding. Myrlin CRISPRi further resulted in pausing of RNA Pol II in the Myb first exon/intron. These data suggest that Myrlin directly participates in activating Myb transcription by recruiting MLL1.
2024-06-11 | GSE240060 | GEO
Project description:Oct4 stemness gene encoding a transcription factor has been shown to overexpress in cancers. However, precise mechanisms of Oct4 relevant to transcriptional reprogramming leading to somatic cancer progression remain unclear. To address the Oct4-mediated transcriptional program in lung cancer, we integrated genome-wide Oct4 binding profiles from chromatin-immunoprecipitation sequencing and ENCODE datasets. We identified that Oct4 occupied at functional promoter and enhancer regions of genes which play key roles in several signaling pathways involving tumorigenesis. Genome-wide Oct4 binding sites were identified via chromatin immunoprecipitation-sequencing analysis of vecoter control and stably Oct4-overexpressing A549 lung cancer cells. ChIP-seq analyses were performed in duplicated samples using Applied Biosystems SOLiD system.
2015-02-04 | E-GEOD-58462 | biostudies-arrayexpress
Project description:Dynamic control of gene expression is critical for blood stage development of malaria parasites. Here, we used multi-omic analyses to investigate transcriptional regulation by the chromatin-associated microrchidia protein, MORC, during asexual blood stage development of the human malaria parasite Plasmodium falciparum. PfMORC (PF3D7_1468100) interacts with a suite of nuclear proteins, including APETALA2 (AP2) transcription factors (PfAP2-G5, PfAP2-O5, PfAP2-I, PF3D7_0420300, PF3D7_0613800, PF3D7_1107800 , and PF3D7_1239200), a DNA helicase DS60 (PF3D7_1227100), and other chromatin remodelers (PfCHD1, PfEELM2, and PfISWI). Transcriptomic analysis of PfMORCHA-glmS knockdown parasites revealed 163 differentially expressed genes belonging to hypervariable multigene families, along with upregulation of genes mostly involved in host cell invasion. In vivo genome-wide chromatin occupancy analysis during both trophozoite and schizont stages of development demonstrates that PfMORC is recruited to repressed, multigene families, including the var genes in subtelomeric chromosomal regions. Collectively, we find that PfMORC is found in chromatin complexes that play a role in the epigenetic control of asexual blood stage transcriptional regulation.
2024-08-14 | PXD044256 | Pride