Satb1 integrates DNA sequence, shape, motif density and torsional stress to selectively bind a subset of putative targets in nucleosome-dense regions of the genome
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ABSTRACT:
PROVIDER: PRJNA508195 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8274690.fastq.gz | Fastqsanger.gz | |||
| SRR8274691.fastq.gz | Fastqsanger.gz | |||
| SRR8274692.fastq.gz | Fastqsanger.gz | |||
| SRR8274693.fastq.gz | Fastqsanger.gz | |||
| SRR8274694.fastq.gz | Fastqsanger.gz |
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Project description:Satb1 (Special AT-rich sequence binding protein 1) coordinates chromatin architecture and regulates a diverse set of cellular and developmental processes. It is not yet clear how Satb1 selects it targets throughout the genome and which cellular parameters modulate its binding landscape. We have used single molecule live cell imaging and deep sequencing to quantify the arrangement of SatB1 molecules in the living nucleus and relate those spatial patterns to specific genomic features. We found that Satb1 preferentially binds to nucleosome dense regions and can access consensus motifs embedded in nucleosomes, features that epitomize 'pioneer' factors. Super-resolution live cell microscopy paired with deep sequencing showed that Satb1 binds iteratively to a set of closely clustered binding sites in the nucleus, and that binding is highly cooperative in regions with high motif density. Further, we observed that Satb1 uses DNA shape information from motif-flanking regions to narrow its binding spectrum. Satb1/DNA interactions were mechanosensitive. Increasing negative torsional stress enhanced binding and Satb1 stabilized base unpairing regions (BURs) against melting by molecular machines such as topoisomerases. Indeed, the ability of a small number of 'master' regulators to control diverse biological programs suggests that these regulators must use a multiparameter, combinatorial logic to select the cell-type and temporally appropriate chromatin state
2019-05-28 | GSE123292 | GEO
Project description:Hematopoietic stem cells (HSCs) are now recognized as a heterogeneous population in self-renewing and differentiation capabilities. However, fundamental mechanisms governing the heterogeneity remain uncertain. We here show that special AT-rich sequence-binding protein 1 (SATB1), a global chromatin organizer, is involved in the mechanisms. Analyzing hematological lineage-restricted SATB1 knock out mice proved that SATB1 is indispensable for both self-renewal and normal differentiation of adult HSCs. Using SATB1/Tomato knock-in mice, we subdivided HSCs according to SATB1 intensity. Culture experiments and RNA-sequencing revealed essential differences between SATB1- and SATB1+ HSCs regarding lineage potential.
2018-06-14 | GSE94630 | GEO
Project description:The Satb1 genome organizer regulates multiple cellular and developmental processes. It is not yet clear how Satb1 selects different sets of targets throughout the genome. Here we have used live-cell single molecule imaging and deep sequencing to assess determinants of Satb1 binding-site selectivity. We have found that Satb1 preferentially targets nucleosome-dense regions and can directly bind consensus motifs within nucleosomes. Some genomic regions harbor multiple, regularly spaced Satb1 binding motifs (typical separation ~1 turn of the DNA helix) characterized by highly cooperative binding. The Satb1 homeodomain is dispensable for high affinity binding but is essential for specificity. Finally, we find that Satb1-DNA interactions are mechanosensitive. Increasing negative torsional stress in DNA enhances Satb1 binding and Satb1 stabilizes base unpairing regions against melting by molecular machines. The ability of Satb1 to control diverse biological programs may reflect its ability to combinatorially use multiple site selection criteria.
| S-EPMC6642133 | biostudies-literature
Project description:Hut78 cell line was used as Sezary syndrome cell model. Comparative transcriptome profiles of SATB1 transduced Hut78 cells (Hut78-SATB1) relative to empty MIG vector transduced control Hut78 cells (Hut78-MIG) were analyzed. The primary goal is to establish a list of genes with differential expression between SATB1 transduced Hut78 cells and control Hut78 cells to identify the gene expression regulation effect of SATB1 expression in Sezary cells. Two color experiment, 3 biological replicates (3 unique cell clones) with Hut78 cells, each compared with a distinct individual clone from cells transduced with empty MIG vector.
2011-12-01 | E-GEOD-24951 | biostudies-arrayexpress
Project description:Hut78 cell line was used as Sezary syndrome cell model. Comparative transcriptome profiles of SATB1 transduced Hut78 cells (Hut78-SATB1) relative to empty MIG vector transduced control Hut78 cells (Hut78-MIG) were analyzed. The primary goal is to establish a list of genes with differential expression between SATB1 transduced Hut78 cells and control Hut78 cells to identify the gene expression regulation effect of SATB1 expression in Sezary cells.
2011-12-01 | GSE24951 | GEO
Project description:Mammalian genomes are organized by multi-layered chromatin folding. How three-dimensional genome organization contributes to cell-type specific transcription remains unclear. We uncover genomic elements termed base-unpairing regions (BURs), distributed genome-wide, as the sole and direct targets of cell-type specific SATB1 protein in vivo. The SATB1 direct-binding profile was generated by analyzing stringently-purified genomic DNA crosslinked to its directly-bound proteins only (ureaChIP-seq). Furthermore, a SATB1-bound BUR interacts extensively and frequently over the entire 5.7 megabase gene-rich region within many regulatory regions, including those near SATB1-dependent Rag1/Rag2 genes. SATB1 depletion leads to major loss of these interactions with greatly reduced Rag1/Rag2 expression. Most BURs reside within lamina associated domains (LADs), among which SATB1 binds to cell-type specific groups of BURs. Genome organization mediated by CTCF and SATB1 are distinct as these proteins do not co-bind chromatin in vivo and their direct binding sites are mutually exclusive genome-wide. These results revealed a previously undetected chromatin organization mediated by SATB1 direct binding to selected BURs genome-wide and suggest that chromatin interactions from some of these BURs provide a regulatory network underlying cell-type specific gene expression.
2021-12-28 | GSE191146 | GEO
Project description:Satb1 and Satb2 are regulators of higher order chromatin in T cells and osteoblasts repectively. We were interested if Satb1 and Satb2 play a role in the regulation of gene expression in ES cells. In this experiment, we compared the transcriptome of wild type and Satb1-/- ES cells. Interestingly Satb1-/- ES cells display an impaired differentiation potential. WT and Satb1-/- ES cells were grown for 3 days in the presence of LIF and selected for Oct4-expression cells by the addition of hygromycin to the culture medium. Previously the cells had been engineered so that they contain a selectable HygroTK reporter in the the Oct4 locus. Total RNA was harvested and used for hybridization.
2009-09-01 | E-GEOD-17487 | biostudies-arrayexpress
Project description:Satb1 and Satb2 are regulators of higher order chromatin in T cells and osteoblasts repectively. We were interested if Satb1 and Satb2 play a role in the regulation of gene expression in ES cells. This SuperSeries is composed of the following subset Series: GSE17487: Expression data in WT and Satb1-/- ES cells GSE17488: Expression data in WT and ES cells overexpressing Satb1 GSE17489: Expression data in WT and ES cells overexpressing Satb2 Refer to individual Series
2009-09-01 | E-GEOD-17490 | biostudies-arrayexpress
Project description:Special AT-rich sequence-binding protein-1 (Satb1) governs genome-wide transcriptional programs. Using a new conditional knockout mouse, we found that Satb1 is required for normal differentiation of conventional dendritic cells (DCs). Furthermore, Satb1 governs the differentiation of inflammatory DCs by regulating MHC-II expression through Notch1 signaling. Mechanistically, Satb1 binds to the Notch1 promoter, activating Notch expression and driving RBPJ occupancy of the H2-Ab1 promoter, which activates MHC-II transcription. However, tumor-driven, unremitting expression of Satb1 in activated Zbtb46+ inflammatory DCs that universally infiltrate ovarian tumors results in an immunosuppressive phenotype characterized by increased secretion of tumor-promoting Galectin-1 and IL-6. Correspondingly, specific in vivo silencing of Satb1 in tumor-associated DCs reverses their tumorigenic activity and boosts protective immunity. Therefore, dynamic fluctuations in Satb1 expression govern the generation and immunostimulatory activity of steady-state and inflammatory DCs, but relentless Satb1 overexpression in differentiated DCs converts them into tolerogenic/pro-inflammatory cells that contribute to malignant progression. RNA-seq with whild type and knocked-down Satb1
2016-01-13 | E-GEOD-76776 | biostudies-arrayexpress
Project description:Satb1 and Satb2 are regulators of higher order chromatin in T cells and osteoblasts repectively. We were interested if Satb1 and Satb2 play a role in the regulation of gene expression in ES cells. In this experiment, we compared the transcriptome of wild type and Satb1-/- ES cells. Interestingly Satb1-/- ES cells display an impaired differentiation potential.
2009-09-01 | GSE17487 | GEO