Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA148505 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR363837.fastq.gz | Fastqsanger.gz | |||
| SRR363838.fastq.gz | Fastqsanger.gz | |||
| SRR363839.fastq.gz | Fastqsanger.gz | |||
| SRR363840.fastq.gz | Fastqsanger.gz | |||
| SRR363841.fastq.gz | Fastqsanger.gz |
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Project description:Acute leukemia are characterized by deregulation of transcriptional networks that control the lineage specificity of gene expression. The aberrant overexpression of the Spi-1/PU.1 transcription factor leads to erythroleukemia. To determine how Spi-1 mechanistically influences the transcriptional program, we combined a ChIP-seq analysis with transcriptional profiling in cells from an erythroleukemic mouse model. We show that Spi-1 displays a selective DNA-binding that does not often cause transcriptional modulation. We report that Spi-1 controls transcriptional activation and repression through distinct Spi-1 recruitment to chromatin. We revealed several parameters impacting on Spi-1-mediated transcriptional activation. Gene activation is facilitated by Spi-1 occupancy close to transcriptional starting site of genes devoid of CGIs. Moreover, in those regions Spi-1 acts by binding to multiple motifs tightly clustered and with similar orientation. Finally, in contrast to the myeloid and lymphoid B cells in which Spi-1 exerts a physiological activity, in the erythroleukemic cells, lineage-specific cooperating factors do not play a prevalent role in Spi-1-mediated transcriptional activation. Thus, our work describes a new mechanism of gene activation through clustered site occupancy of Spi-1 particularly relevant in regard to the strong expression of Spi-1 in the erythroleukemic cells.
2012-06-30 | GSE33611 | GEO
Project description:Acute leukemia are characterized by deregulation of transcriptional networks that control the lineage specificity of gene expression. The aberrant overexpression of the Spi-1/PU.1 transcription factor leads to erythroleukemia. To determine how Spi-1 mechanistically influences the transcriptional program, we combined a ChIP-seq analysis with transcriptional profiling in cells from an erythroleukemic mouse model. We show that Spi-1 displays a selective DNA-binding that does not often cause transcriptional modulation. We report that Spi-1 controls transcriptional activation and repression through distinct Spi-1 recruitment to chromatin. We revealed several parameters impacting on Spi-1-mediated transcriptional activation. Gene activation is facilitated by Spi-1 occupancy close to transcriptional starting site of genes devoid of CGIs. Moreover, in those regions Spi-1 acts by binding to multiple motifs tightly clustered and with similar orientation. Finally, in contrast to the myeloid and lymphoid B cells in which Spi-1 exerts a physiological activity, in the erythroleukemic cells, lineage-specific cooperating factors do not play a prevalent role in Spi-1-mediated transcriptional activation. Thus, our work describes a new mechanism of gene activation through clustered site occupancy of Spi-1 particularly relevant in regard to the strong expression of Spi-1 in the erythroleukemic cells. Chromatin immunoprecipitations of Spi-1, H3K36me3, RNApolII,mouse IgG followed by sequencing were performed on spleen-derived erythroleukemic cells of spi-1 transgenic mice. In case of Spi-1, reads obtained from the two different mice represent biological replicates and were merged for bioinformatic analysis. Input DNA from each ChIP experiments have been pooled and sequenced as one control.
2012-06-30 | E-GEOD-33611 | biostudies-arrayexpress
Project description:Spi-B and PU.1 are highly related members of the E26-transformation-specific (ETS) family of transcription factors that have similar, but not identical, functions in B cell development. PU.1 and Spi-B are both expressed at high levels in lymphoma cell lines. We hypothesized that Spi-B and PU.1 occupy similar sites in the genome. To determine binding sites of Spi-B and PU.1, WEHI-279 mouse lymphoma cells were infected with retroviral vectors encoding 3XFLAG-tagged PU.1 or Spi-B. Anti-FLAG chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq) was performed. Both transcription factors occupied approximately 2000 sites in the genome, and approximately half of these sites were bound by both factors while the other sites were unique to each factor.
2014-11-10 | GSE58128 | GEO
Project description:A network of long-range interactions between functional DNA elements regulates gene expression in a precise spatio-temporal pattern during development. We carried out anti-RNA polymerase II and cohesin ChIA-PET and DNase-seq in Mouse Erythroleukemia (MEL) cells to capture genome-wide changes between open chromatin elements in chromatin interaction graphs (CIGs) during DMSO-induced hemoglobin activation. We found that the change of interaction strength in CIGs is positively correlated to expression changes in corresponding genes as measured by RNA-seq. DNaseI footprints and ChIP-seq data indicate that these long-range interactions are controlled through distinct combinations of transcription factors before and after differentiation, with CTCF or cohesin only mediating half of these interactions, with GATA1, PU.1 and/or other transcription factorsYY1 interactions accounting for an additional 40% of detected interactions. Strikingly, while CTCF and GATA1–mediated interactions were enriched in genes involved in erythrocyte differentiation and mitochondrial regulation, PU.1YY1-mediated interactions were enriched for genes involved in RNA processing, cell cycletranslation, and chromatin organizationhistone remodeling. We further found that two-thirds of MEL DNA elements with long-range interactions as well as 35% of their interactions are conserved in human K562 cells and they show similar combinations of factor occupancy in both species. Our study highlights the importance of quantitative analysis of changes in long-range interaction strengths in quantifying changes in gene expression.
2020-02-29 | GSE110361 | GEO
Project description:Deletion of genes encoding the E26 transformation-specific (ETS) transcription factors, PU.1 and Spi-B, in B cells (CD19-CreDPB mice) leads to acute lymphoblastic leukemia at 100% incidence and with a median survival of 21 weeks. To identify pathways of leukemic transformation, we compared gene expression in leukemia cells from CD19-CreDPB mice (CD19-CreDPB B220- B-ALL) with B cells from Spi-B knockout (Control DB) or B cells from CD19-CreDPB mice (CD19-CreDPB B220+ B cell)
2014-11-12 | GSE48891 | GEO
Project description:Co-regulation of transcription factor binding and nucleosome occupancy through DNA features of mammalian enhancers
| PRJNA218857 | ENA
Project description:A major problem with linking transcription factor binding to function is that many factors bind to a large number of, at least in any given cell type, seemingly irrelevant regions. This makes it hard to filter out which binding sites are responsible for the regulation of a given gene. PU.1 (Spi1, Sfpi1) is an excellent example of a transcription factor that works both to mediate developmental choices and to serve the alternative developmental fates that emerge from these choices. Its role in T-cell development is confined to the early stages where high PU.1 expression persists through multiple cell divisions and is sharply downregulated over the DN2a-to-DN2b T-cell commitment stage. Even though it is known that PU.1 is necessary for the survival of the earliest T-cell progenitors, where it is needed for optimal proliferation, control of alternative lineage genes, and correct timing of the access to T-lineage genes, it has not been well-studied how PU.1 finds it targets and exerts its functions within this context. Here, we show in detail how PU.1 selects its binding sites and subsequently regulate gene expression. We show that PU.1 has two effective affinity thresholds for occupancy depending on current chromatin openness as measured by ATAC-sequencing, but that it is easily capable of binding sites in closed chromatin. Unexpectedly, although its binding to promoters is least constrained, promoters are the only major class of sites where it exerts a predominantly negative effect; otherwise it works locally as an activator, mainly mediated through binding to sites in closed or dynamically closing distal enhancer elements, where it can rapidly open chromatin and induce histone acetylation. However, its ability to open the chromatin depends not only on its own affinity but also on the presence of collaborating factors, because we show that PU.1 introduction into PU.1-negative cells triggers a massive reorganization of occupancy patterns of at least three other factors: Runx1, Satb1, and Gata3. Most strikingly, PU.1’s “theft” of Runx1 and Satb1 from many sites where they were binding in the absence of PU.1 enables PU.1 to exert a novel form of repression even on genes where it has no binding sites itself. We show here that PU.1 requires domains outside of its DNA binding domain to properly open chromatin, and this structural requirement is directly connected with its ability to bind to Runx1 and to Satb1, and moreover, Runx1, in particular, is an important collaborator to activate many of its target genes in the context of early T-cell development. Thus, PU.1 regulates gene expression via two distinct mechanisms. First, PU.1 steals Satb1 and Runx1 from many genomic sites, thereby repressing T cell gene expression indirectly. Second, PU.1, opens chromatin, recruits Satb1 and Runx1 to new sites, and directly activates its target gene expression. In summary, we here present a model where a transcription factor can work through redeployment of other factors and not only through sites that it binds itself.
2018-06-21 | GSE93755 | GEO
Project description:PU.1 is a prototype master transcription factor (TF) of hematopoietic cell differentiation with diverse roles in different lineages. Analysis of its genome-wide binding pattern across PU.1 expressing cell types revealed manifold cell type-specific binding patterns. They are not consistent with the epigenetic and chromatin constraints to PU.1 binding observed in vitro, suggesting that PU.1 requires auxiliary factors to access DNA in vivo. Using a model of transient mRNA expression we show that PU.1 induction leads to the extensive remodeling of chromatin, redistribution of partner transcription factors and rapid initiation of a myeloid gene expression program in heterologous cell types. By probing PU.1 mutants for defects in chromatin access and screening for PU.1 proximal proteins in vivo, we found that its N-terminal acidic domain was required for the recruitment of SWI/SNF remodeling complexes, de novo chromatin access and stable binding as well as the redistribution of partner TFs.
2019-11-20 | PXD013167 | Pride
Project description:ETS trancription factors PU.1 and Spi-B binding in mouse lymphoma cells
| PRJNA249085 | ENA
Project description:We find that the myeloid master regulatory transcription factor, PU.1, binds to >16,000 sites in both normal and leukemic erythroid cells. Of these bound sites, ~7,000 lie within 2kb of TSS of a gene, suggesting PU.1 may regulate a large number of genes in erythroid cells. Coupling this data with gene expression analysis, we show PU.1 directly regulates several critical signaling pathways in erythroid cells. Assaying PU.1 occupancy in normal and leukemic erythroid cells
2011-06-23 | E-GEOD-21950 | biostudies-arrayexpress