Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA208892 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1171520.fastq.gz | Fastqsanger.gz | |||
| SRR1171521.fastq.gz | Fastqsanger.gz | |||
| SRR908253.fastq.gz | Fastqsanger.gz | |||
| SRR908254.fastq.gz | Fastqsanger.gz | |||
| SRR908255.fastq.gz | Fastqsanger.gz |
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Project description:Genome-scale analysis in blood progenitor and mast cells reveals how lineage-affiliated transcription factors control distinct regulatory programs [Beadchip Experiments]
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Project description:Genome-scale analysis in blood progenitor and mast cells reveals how lineage-affiliated transcription factors control distinct regulatory programs [Beadchip Experiments #2]
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Project description:In development, pioneer transcription factors access silent chromatin to reveal lineage-specific gene programs. The structured DNA-binding domains of pioneer factors have been well characterized, but whether and how low-complexity intrinsically disordered regions (IDRs) affect chromatin and control cell fate is unclear. Here, we report deletion of an IDR of the pioneer factor TCF-1, termed “L1”, leads to an early developmental block in T cells. The few T cells that develop from progenitors expressing TCF-1 lacking L1 exhibit lineage infidelity distinct from the lineage diversion of TCF-1 deficient cells. Mechanistically, L1 is required for activation of T cell genes and de-repression of GATA2 driven genes, normally reserved to the mast cell and dendritic cell lineages. Underlying this lineage diversion, L1 mediates binding of TCF-1 to its earliest target genes which are subject to repression as T cells develop. These data suggest TCF-1’s intrinsically disordered N-terminus maintains T cell lineage fidelity.
2024-06-16 | PXD043586 | Pride
Project description:Recent studies have revealed the importance of long noncoding RNAs (lncRNAs) as tissue-specific regulators of gene expression. There is ample evidence that distinct types of vasculature undergo tight transcriptional control to preserve their structure, identity, and functions. We determined, for the first time, the global lineage-specific lncRNAome of human dermal blood and lymphatic endothelial cells (BECs and LECs), combining RNA-Seq and CAGE-Seq. A subsequent genome-wide antisense oligonucleotide-knockdown profiling of two BEC- and two LEC-specific lncRNAs identified LETR1 as a critical gatekeeper of the global LEC transcriptome. Deep RNA-DNA and RNA-protein interaction studies, and phenotype rescue analyses revealed that LETR1 is a nuclear trans-acting lncRNA modulating, via key epigenetic factors, the expression of essential target genes governing the growth and migratory ability of LECs. Together, our study provides new evidence supporting the intriguing concept that every cell type expresses precise lncRNA signatures to control lineage-specific regulatory programs.
2020-12-21 | PXD018578 | Pride
Project description:<p>Most pancreatic neuroendocrine tumors (PNETs) do not produce symptoms of hormonal excess and are hence considered “non-functional”. Their clinical behaviors vary widely, emphasizing the need for a robust classification with prognostic power. Using enhancer maps to infer regulatory programs, we find that the large majority of non-functional PNETs fall into two major sub-types that reflect alpha and beta endocrine cell ontogeny, respectively. Tumors of the different subtypes have similar clinical presentations and histology, but express distinct lineage-specifying transcription factors, ARX or PDX1. Here we provide the raw ChIP-seq and RNA-seq data of the PNET cohort in this study, as well as ChIP-seq data of ileal carcinoids.</p>
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Project description:The myeloid innate immune system plays key roles in the defence against parasites and bacteria, and carries out essential functions during tissue homeostasis and repair. It consist of neutrophils, macrophages, eosinophils, basophils and mast cells. Myelopoietic dysfunction or deregulation underlies numerous pathologies, ranging from immune deficiencies and allergies to myeloproliferative disorders and myeloid leukemia. To study malignant myelopoiesis, it is essential to understand the ontology of the different celltypes. In a generally accepted model for hematopoietic differentiation, all myeloid cells are preceded by a common granulocyte and macrophage progenitor that has the potential for all myeloid celltypes at the single cell level. However, we recently proposed a model for mouse hematopoiesis in which myeloid cells are formed via two independent pathways, one leading towards macrophages and neutrophils and one leading towards eosinophils, basophils and mast cells. The first pathway is affiliated with lymphoid potentials whereas the latter with megakaryocyte/erythroid development. Here, we demonstrate that those findings translate to human hematopoiesis. We demonstrate prospective isolation of myeloid progenitor cells that have restricted multipotent myeloid potential and are affiliated with lineages similar to those found in the mouse hierarchy.
2019-03-27 | GSE113046 | GEO
Project description:The emerging notion of hematopoietic stem- and progenitor cells (HSPCs) as a low-primed cloud without sharply demarcated gene expression programs raises the question on how cellular fate options emerge, and at which stem-like stage lineage priming is initiated. Here we investigated single-cell chromatin accessibility of Lineage-, cKit+, Sca1+ (LSK) HSPCs spanning the early differentiation landscape. Application of a signal-processing algorithm to detect transition points corresponding to massive alterations in accessibility of 521 transcription factor-motifs revealed a population of LSK FMS-like tyrosine kinase 3(Flt3)intCD9high cells that concurrently display stem-like and lineage-affiliated chromatin signatures pointing to simultaneous gain of both Lympho-Myeloid and Megakaryocyte-Erythroid programs. Molecularly and functionally, these cells position between stem cells and committed progenitors, display multi-lineage capacity in vitro and in vivo, but lack self-renewal activity. This integrative molecular analysis resolves the heterogeneity of cells along hematopoietic differentiation trajectories, and permits investigation of chromatin-mediated transition between multipotency and lineage restriction.
2022-05-02 | GSE148746 | GEO
Project description:Despite major advances in the generation of genome-wide binding maps, the mechanisms by which transcription factors (TFs) regulate cell type identity have remained largely obscure. Through comparative analysis of 10 key haematopoietic TFs in both mast cells and blood progenitors, we demonstrate that the largely cell-type specific binding profiles are not opportunistic, but instead contribute to cell-type specific transcriptional control, because (1) mathematical modelling of differential binding of shared TFs can explain differential gene expression, (2) cell-type specific binding is largely mediated through consensus binding sites, and (3) knock-down of blood stem cell regulators Gata2 and Erg in mast cells reveals mast cell specific genes as direct targets. Finally we show that the known mast cell regulators Mitf and c-Fos likely contribute to the global reorganisation of TF binding profiles. Taken together therefore, our study elucidates how key regulatory TFs contribute to transcriptional programmes in several distinct mammalian cell types. Comparison of HPC7 cell line (haematopoietic multipotent progenitor) and primary mast cells. 10 key haematopoietic transcription factors and mRNA expression were profiled in both cell types.
2014-04-24 | E-GEOD-48085 | biostudies-arrayexpress