Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA385830 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5516290.fastq.gz | Fastqsanger.gz | |||
| SRR5516291.fastq.gz | Fastqsanger.gz | |||
| SRR5516282.fastq.gz | Fastqsanger.gz | |||
| SRR5516292.fastq.gz | Fastqsanger.gz | |||
| SRR5516283.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 11 |
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Project description:Helper innate lymphoid cells (ILC) play important functions in immunity and tissue homeostasis, but their development remains poorly understood. In this study, we identified NFIL3 as the earliest known requirement during ILC development. Forced expression of NFIL3 in mouse lymphoid progenitors in vitro triggered the staged expression of downstream transcription factors including Tcf7, Gata3, Zbtb16 and Id2 that are implicated in ILC development. Thus, NFIL3 resides at the apex of a hierarchy of transcription factors important for innate lymphocyte development, and is necessary and sufficient to impose the innate lymphoid cell fate.
2025-10-30 | GSE291321 | GEO
Project description:Helper innate lymphoid cells (ILC) play important functions in immunity and tissue homeostasis, but their development remains poorly understood. In this study, we identified NFIL3 as the earliest known requirement during ILC development. Forced expression of NFIL3 in mouse lymphoid progenitors in vitro triggered the staged expression of downstream transcription factors including Tcf7, Gata3, Zbtb16 and Id2 that are implicated in ILC development. Thus, NFIL3 resides at the apex of a hierarchy of transcription factors important for innate lymphocyte development, and is necessary and sufficient to impose the innate lymphoid cell fate.
2025-10-30 | GSE291319 | GEO
Project description:Helper innate lymphoid cells (ILC) play important functions in immunity and tissue homeostasis, but their development remains poorly understood. In this study, we identified NFIL3 as the earliest known requirement during ILC development. Forced expression of NFIL3 in mouse lymphoid progenitors in vitro triggered the staged expression of downstream transcription factors including Tcf7, Gata3, Zbtb16 and Id2 that are implicated in ILC development. Thus, NFIL3 resides at the apex of a hierarchy of transcription factors important for innate lymphocyte development, and is necessary and sufficient to impose the innate lymphoid cell fate.
2025-10-30 | GSE291317 | GEO
Project description:Helper innate lymphoid cells (ILC) play important functions in immunity and tissue homeostasis, but their development remains poorly understood. In this study, we identified NFIL3 as the earliest known requirement during ILC development. Forced expression of NFIL3 in mouse lymphoid progenitors in vitro triggered the staged expression of downstream transcription factors including Tcf7, Gata3, Zbtb16 and Id2 that are implicated in ILC development. Thus, NFIL3 resides at the apex of a hierarchy of transcription factors important for innate lymphocyte development, and is necessary and sufficient to impose the innate lymphoid cell fate.
2025-10-30 | GSE291316 | GEO
Project description:Helper innate lymphoid cells (ILC) play important functions in immunity and tissue homeostasis, but their development remains poorly understood. In this study, we identified NFIL3 as the earliest known requirement during ILC development. Forced expression of NFIL3 in mouse lymphoid progenitors in vitro triggered the staged expression of downstream transcription factors including Tcf7, Gata3, Zbtb16 and Id2 that are implicated in ILC development. Thus, NFIL3 resides at the apex of a hierarchy of transcription factors important for innate lymphocyte development, and is necessary and sufficient to impose the innate lymphoid cell fate.
2025-10-30 | GSE291076 | GEO
Project description:Helper innate lymphoid cells (ILC) play important functions in immunity and tissue homeostasis, but their development remains poorly understood. In this study, we identified NFIL3 as the earliest known requirement during ILC development. Forced expression of NFIL3 in mouse lymphoid progenitors in vitro triggered the staged expression of downstream transcription factors including Tcf7, Gata3, Zbtb16 and Id2 that are implicated in ILC development. Thus, NFIL3 resides at the apex of a hierarchy of transcription factors important for innate lymphocyte development, and is necessary and sufficient to impose the innate lymphoid cell fate.
2025-10-30 | GSE291075 | GEO
Project description:<p>Transcription factor p63 is a key regulator of epidermal keratinocyte proliferation and differentiation. Mutations in the p63 DNA-binding domain are associated with Ectrodactyly Ectodermal Dysplasia Cleft Lip/Palate (EEC) syndrome. Underlying molecular mechanism of these mutations however remain unclear. Here we characterized the transcriptome and epigenome of p63 mutant keratinocytes derived from EEC patients. The transcriptome of p63 mutant keratinocytes deviated from the normal epidermal cell identity. Epigenomic analyses showed an altered enhancer landscape in p63 mutant keratinocytes contributed by loss of p63-bound active enhancers and by unexpected gain of enhancers. The gained enhancers were frequently bound by deregulated transcription factors such as RUNX1. Reversing RUNX1 overexpression partially rescued deregulated gene expression and the altered enhancer landscape. Our findings identify an unreported disease mechanism whereby mutant p63 rewires the enhancer landscape and affects epidermal cell identity, consolidating the pivotal role of p63 in controlling the enhancer landscape of epidermal keratinocytes.</p>
| phs001737 | dbGaP
Project description:Transcription factor (TF) reporter mice have proved integral to the characterization of murine innate lymphoid cell (ILC) development and function. Here, we implemented a CRISPR/Cas9-generated combinatorial reporter approach for the simultaneous resolution of several key TFs throughout ILC development in both the fetal liver and adult bone marrow. We demonstrate that the Tcf7-expressing early innate lymphoid progenitor (EILP) and the common helper innate lymphoid progenitor (CHILP) both contain a heterogeneous mixture of committed ILC and Lymphoid Tissue-inducer (LTi) precursors, rather than a shared precursor to these lineages. Moreover, the earliest specified precursor to the LTi lineage was identified upstream of these populations, prior to the expression of Tcf7. These findings match dynamic changes in chromatin accessibility associated with the expression of key TFs (ie. Gata3 and Rorc), highlighting the distinct origins of ILC and LTi lineages at the epigenetic and functional levels, and provide a revised map for ILC development.
2020-09-28 | GSE150763 | GEO
Project description:Innate lymphoid cells (ILCs) are recently identified lymphocytes that limit infection and promote tissue repair at mucosal surfaces. However, the pathways underlying ILC development remain unclear. Here we show that the transcription factor NFIL3 directs the development of a committed bone marrow precursor that differentiates into all known ILC lineages. NFIL3 was required in the common lymphoid progenitor (CLP), and was essential for the differentiation of CLP, a bone marrow cell population that gives rise to all known ILC lineages. Clonal differentiation studies revealed that CXCR6+ cells within the CLP population differentiate into all ILC lineages but not T- and B-cells. We further show that NFIL3 governs ILC development by directly regulating expression of the transcription factor TOX. These findings establish that NFIL3 directs the differentiation of a committed ILC precursor that gives rise to all ILC lineages and provide insight into the defining role of NFIL3 in ILC development. This experiment is to compare gene expression profiles between wild-type and Nfil3-/- common lymphoid progenitor (CLP) cells to identify genes regulated by NFIL3. There are 6 samples in this experiment, including 3 biological replicates for wild-type CLPs and 3 biological replicates for Nfil3-/- CLPs. All mice used are on the C57BL/6 background.
2014-10-16 | E-GEOD-62337 | biostudies-arrayexpress
Project description:The hematopoietic master regulator RUNX1 is frequently mutated in myeloid and lymphoid malignancies. Analyses of RUNX1 mutations across hematopoietic tissues revealed frequent mutations outside of the N-terminal DNA binding domain. The vast majority of these C-terminal mutations were found to be nonsense and frameshifts resulting in truncated protein products predicted to escape nonsense mediated decay pathways. We modeled this class of truncation mutation using the pathogenic RUNX1 R320* mutation found in both germline and sporadic hematological disease. Homozygous knock-in of RUNX1 R320* in K562 leukemia cells resulted in a megakaryocytic differentiation block and DNA damage sensitivity phenotypes. Gene expression analysis demonstrated that RUNX1 R320* dysregulated unique gene sets when compared to RUNX1 knockdown in addition to shared genes related to megakaryocyte and platelet function. DNA binding across the genome was examined between RUNX1 wild-type and RUNX1 R320* through ChIP-seq, revealing that RUNX1 R320* differential binding was most enriched at enhancer regions. To detect RUNX1 R320* dysregulated enhancer-promoter (E-P) connections we performed GRID-seq and uncovered extensive remodeling of E-P interactions genome-wide in RUNX1 R320* cells. Furthermore, we uncovered a novel role for FOXK2 at RUNX1 regulated enhancers. Analysis of the well-studied MYC enhancer region demonstrated cooperation between RUNX1 R320* and FOXK2 at hematopoietic MYC enhancers NDME and BENC resulting in the significant upregulation of the MYC oncogene. In conclusion, the truncation of RUNX1 results in impaired megakaryocytic differentiation, unique transcriptional alterations, and remodeling of enhancer-promoter connections in cooperation with FOXK2, together contributing to leukemogenesis.
2024-05-29 | GSE236641 | GEO