Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA217417 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR958946.fastq.gz | Fastqsanger.gz | |||
| SRR958947.fastq.gz | Fastqsanger.gz | |||
| SRR958948.fastq.gz | Fastqsanger.gz | |||
| SRR958949.fastq.gz | Fastqsanger.gz | |||
| SRR958950.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 17 |
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Project description:Dynamic analysis of gene expression and genome wide transcription factor binding during lineage-specification of multipotent progenitors [HP]
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Project description:Dynamic analysis of gene expression and genome wide transcription factor binding during lineage-specification of multipotent progenitors [ER]
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Project description:Dynamic analysis of gene expression and genome wide transcription factor binding during lineage-specification of multipotent progenitors [TC]
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Project description:Dynamic analysis of gene expression and genome wide transcription factor binding during lineage-specification of multipotent progenitors [PC]
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Project description:Tcf1 is necessary for optimal T lineage development. Tcf1 deficient progenitors fail to initiate the T lineage program in vitro and development is severely defective in vivo. We used microarrays to assess the overal global gene expression differences from Tcf1 wildtype and deficient lymphoid biased progenitors cultures on Notch-ligand expressing stroma to determine if Tcf1 deficient progenitors are able to intiate the T lineage specification program. Abstract of manuscript: The thymus imposes the T cell fate on incoming multipotent progenitors, but the molecular mechanisms are poorly understood. We show that transcription factor Tcf1 initiates T-lineage-specific gene expression. Tcf1 is downstream of Notch1 signaling and expressed in early T-cell progenitors. Progenitors deficient for Tcf1 are unable to initiate normal T-lineage specification. Conversely, ectopic expression of Tcf1 in hematopoietic progenitors is sufficient to induce expression of T-lineage specific genes in vitro. Thus, our study identifies Tcf1 as critically involved in the establishment T cell identity. Tcf1 wildtype and deficient bone marrow lymphoid primed progenitors (LMPPs, Lineage marker- Sca+kit+Flt3high) were harvested in triplicate and seeded onto OP9-DL4 expressing stroma for 4 days upon which highly pure lineage negative and Thy1+CD25+ T cells were cell sorted for expression analysis. The lineage negative populations represent three seperate mice from each genotype and the Thy1+CD25+T lineage population represents two replicates from the Tcf1 wildtype group. No Thy1+CD25+ T lineage cells develop from Tcf1 deficient progentiors.
2011-08-03 | E-GEOD-26559 | biostudies-arrayexpress
Project description:Collombet2016 - Lymphoid and myeloid cell
specification and transdifferentiation
This model is described in the article:
Logical modeling of lymphoid
and myeloid cell specification and transdifferentiation
Samuel Collombet, Chris van Oevelen,
Jose Luis Sardina Ortega, Wassim Abou-Jaoudé, Bruno Di
Stefano, Morgane Thomas-Chollier, Thomas Graf, and Denis
Thieffry
Proceedings of the National Academy of
Sciences of the United States of America
Abstract:
Blood cells are derived from a common set of hematopoietic
stem cells, which differentiate into more specific progenitors
of the myeloid and lymphoid lineages, ultimately leading to
differentiated cells. This developmental process is controlled
by a complex regulatory network involving cytokines and their
receptors, transcription factors, and chromatin remodelers.
Using public data and data from our own molecular genetic
experiments (quantitative PCR, Western blot, EMSA) or
genome-wide assays (RNA-sequencing, ChIP-sequencing), we have
assembled a comprehensive regulatory network encompassing the
main transcription factors and signaling components involved in
myeloid and lymphoid development. Focusing on B-cell and
macrophage development, we defined a qualitative dynamical
model recapitulating cytokine-induced differentiation of common
progenitors, the effect of various reported gene knockdowns,
and the reprogramming of pre-B cells into macrophages induced
by the ectopic expression of specific transcription factors.
The resulting network model can be used as a template for the
integration of new hematopoietic differentiation and
transdifferentiation data to foster our understanding of
lymphoid/myeloid cell-fate decisions.
This model is hosted on
BioModels Database
and identified by:
MODEL1610240000.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2017-06-08 | MODEL1610240000 | BioModels
Project description:Tcf1 is necessary for optimal T lineage development. Tcf1 deficient progenitors fail to initiate the T lineage program in vitro and development is severely defective in vivo. We used microarrays to assess the overal global gene expression differences from Tcf1 wildtype and deficient lymphoid biased progenitors cultures on Notch-ligand expressing stroma to determine if Tcf1 deficient progenitors are able to intiate the T lineage specification program. Abstract of manuscript: The thymus imposes the T cell fate on incoming multipotent progenitors, but the molecular mechanisms are poorly understood. We show that transcription factor Tcf1 initiates T-lineage-specific gene expression. Tcf1 is downstream of Notch1 signaling and expressed in early T-cell progenitors. Progenitors deficient for Tcf1 are unable to initiate normal T-lineage specification. Conversely, ectopic expression of Tcf1 in hematopoietic progenitors is sufficient to induce expression of T-lineage specific genes in vitro. Thus, our study identifies Tcf1 as critically involved in the establishment T cell identity.
2011-08-04 | GSE26559 | GEO
Project description:The transcription factor BRACHYURY (T, BRA) is one of the first markers of gastrulation and lineage specification in mammals. Despite its wide use and importance in stem cell and developmental biology, its genomic targets are largely unknown. Here, we used differentiated human embryonic stem cells to study the role of BRA in Bmp4-induced mesoderm and Activin-induced endoderm progenitors by ChIP-seq. We show that BRA has distinct genome-wide binding landscapes in these two populations. Our data illuminate the function of BRA in the context of human embryonic development and show that the regulatory role of BRA is context-dependent. ChIP-seq of BRACHYURY (T, BRA) in two cell types: endoderm and mesoderm progenitors derived from human embryonic stem cells after 36 hours of growth in chemically-defined media (described in Bernardo et al., Cell Stem Cell, 2011, 9:144-155). Input DNA samples are included as a control.
2015-05-18 | E-GEOD-60606 | biostudies-arrayexpress
Project description:B-lymphocyte development is dependent on the interplay between the chromatin landscape and lineage specific transcription factors. It has been suggested that B-lineage commitment is associated with major changes in the nuclear chromatin environment proposing a critical role for lineage specific transcription factors in the formation of the epigenetic landscape. In this report we have used chromosome conformation capture in combination with ATAC-seq analysis to enable highly efficient annotation of both proximal and distal transcriptional control elements to genes activated in B-lineage specification. A large majority of these genes were annotated to at least one regulatory element with an accessible chromatin configuration in multipotent progenitors. Furthermore, the majority of binding sites for the key regulators of B-lineage specification, EBF1 and PAX5, occurred in already accessible regions. EBF1 did, however, cause a dynamic change in ATAC-accessibility and was critical for an increase in distal promoter-enhancer interactions as well as high deposition of chromatin modulating co-factors associated with the establishment of the B-lineage program. Our data unravel an unappreciated level of epigenetic priming at regulatory elements annotated to lineage restricted genes and provide insight into the mechanisms by which lineage specific transcription factors act via already accessible elements in lineage specification.
2021-05-31 | GSE162858 | GEO