Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA106999 | ENA |
REPOSITORIES: ENA
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Project description:Foxo1 and Ebf1 deficiency leads to a similar disruption of normal B-cell development at the level of the common lymphoid progenitor (CLP). Both mouse strains display the existance of LY6D+ CLPs but a marked/complete lack of proB cells. To investigate similarities of the developmental defects observed we generated gene expression profiles from both genotypes (with corresponding WT controls). This illustrated a shared gene expression signature in Ebf1/Foxo1 deficient CLPs. Gene expression profiling was done using highly purified (FACS sorted) progenitor cells. Cells were purified from bone marrow of wild-type, Foxo1 deficient and Ebf1 deficient mice. Ebf1 deficient bone marrow was aquired by transplantation of Ebf1 deficient progenitors into irradiated hosts. Populations analysed were CLP LY6D-, CLP LY6D+ and proB cells.
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Project description:Gene expression profiling was performed of Pax5 wild type bone marrow subsets from common lymphoid progenitors through to Hardy stage F cells. These cells were obtained by flow sorting of bone marrow. Gene expression profiling was performed on 41 samples of RNA extracted from flow sorted B cell precursor populations from common lymphoid progenitor (CLP) through to Hardy stage F. Note that several of the genes expressed in normal mouse B cell progenitors are also involved by deletion/mutation in hypodiploid ALL. Related hypodiploid ALL studies: Gene expression data: GEO GSE27237 SNP & Sequencing data: dbGaP phs000341.v1.p1
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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.
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