Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA227282 | ENA |
REPOSITORIES: ENA
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Project description:The zinc finger transcription factor GATA1 plays an essential role for differentiation in several hematopoietic cell lineages including erythroid cells, megakaryocytes and eosinophils. Although some studies demonstrated that GATA1 is also required for mast cell differentiation, the effect of complete ablation of GATA1 in mast cell differentiation has not been examined. Here, by using tamoxifen-inducible conditional Gata1 knockout mice, we show that the role of GATA1 in mast cell differentiation is less than previously anticipated in adult mice. Although systemic administration of tamoxifen resulted in complete ablation of GATA1 protein in bone marrow and spleen, cell number and distribution of peripheral tissue mast cells in Gata1-null mice were comparable to those in wild type mice. Bone marrow cells derived from Gata1-null mice differentiated into mast cells that express both c-Kit and IgE receptor α subunit. Finally, we show a line of evidence that GATA1 and GATA2 cooperatively regulate the expression of several mast cell-specific genes by chromatin immunoprecipitation assays and quantitative RT-PCR analyses. These results indicate that GATA1 is dispensable for differentiation and maintenance of mast cells in postnatal hematopoiesis and the loss of GATA1 function is likely compensated by GATA2.
2014-03-02 | GSE52254 | GEO
Project description:The zinc finger transcription factor GATA1 plays an essential role for differentiation in several hematopoietic cell lineages including erythroid cells, megakaryocytes and eosinophils. Although some studies demonstrated that GATA1 is also required for mast cell differentiation, the effect of complete ablation of GATA1 in mast cell differentiation has not been examined. Here, by using tamoxifen-inducible conditional Gata1 knockout mice, we show that the role of GATA1 in mast cell differentiation is less than previously anticipated in adult mice. Although systemic administration of tamoxifen resulted in complete ablation of GATA1 protein in bone marrow and spleen, cell number and distribution of peripheral tissue mast cells in Gata1-null mice were comparable to those in wild type mice. Bone marrow cells derived from Gata1-null mice differentiated into mast cells that express both c-Kit and IgE receptor M-NM-1 subunit. Finally, we show a line of evidence that GATA1 and GATA2 cooperatively regulate the expression of several mast cell-specific genes by chromatin immunoprecipitation assays and quantitative RT-PCR analyses. These results indicate that GATA1 is dispensable for differentiation and maintenance of mast cells in postnatal hematopoiesis and the loss of GATA1 function is likely compensated by GATA2. Murine bone marrow-derived mast cells from C57BL/6 mice were transfected with of control or GATA1 siRNA (200 pmol). Two samples were analyzed. Sample1 (ctrsi-mix) is prepared from cells transfected with control siRNA. Sample2 (G1si-mix) is prepared from cells transfected with GATA1 siRNA. For each siRNA treatment, two replicate samples prepared from different animals were pooled and used for the analysis.
2014-03-02 | E-GEOD-52254 | biostudies-arrayexpress
Project description:Gene expression during cellular differentiation is coordinated by combinatorial interactions between transcription factors (TFs) and cofactors at promoters and enhancers. The “master TF” GATA1 coordinates gene transcription in a subset of hematopoietic lineages, including erythroid, megakaryocytic, mast, and eosinophil, while repressing the development of other blood lineages. However, the specific cofactors required for GATA1-activated gene expression during hematopoiesis are incompletely defined. We identified the cofactor KMT2D, an H3K4 methyltransferase that collaborates with H3K27 acetyltransferases to activate transcription, in an unbiased CRISPR/Cas9 screen for epigenetic regulators of erythropoiesis. Loss of KMT2D in human erythroid precursors caused developmental arrest with impaired expression of numerous erythroid genes. Mechanistically, KMT2D colocalized with GATA1 on more than one thousand erythroid enhancers associated with over two hundred erythroid genes. In general, co-occupancy of GATA1 and KMT2D at erythroid enhancers was associated with stronger transcriptional activity than occupancy by GATA1 alone. Acute depletion of KMT2D in erythroid precursors caused rapid reductions of H3K4me1 and H3K27ac on a subset of GATA1-bound enhancers and impaired the expression of canonical erythroid genes, including ZFPM1, SLC4A1, and EPOR. Moreover, acute depletion of GATA1 or KMT2D individually caused downregulation of overlapping gene sets. Thus, KMT2D controls erythropoiesis by selectively activating GATA1-dependent erythroid enhancers. Our studies identify KMT2D as a novel cofactor for transcriptional activation by GATA1 during erythropoiesis. More generally, our findings demonstrate how a lineage-specific TF cooperates with a ubiquitous epigenetic regulator to drive lineage-specific gene expression during cellular differentiation.
2026-04-10 | PXD076443 | Pride
Project description:PURPOSE: To provide a detailed gene expression profile of the normal postnatal mouse cornea. METHODS: Serial analysis of gene expression (SAGE) was performed on postnatal day (PN)9 and adult mouse (6 week) total corneas. The expression of selected genes was analyzed by in situ hybridization. RESULTS: A total of 64,272 PN9 and 62,206 adult tags were sequenced. Mouse corneal transcriptomes are composed of at least 19,544 and 18,509 unique mRNAs, respectively. One third of the unique tags were expressed at both stages, whereas a third was identified exclusively in PN9 or adult corneas. Three hundred thirty-four PN9 and 339 adult tags were enriched more than fivefold over other published nonocular libraries. Abundant transcripts were associated with metabolic functions, redox activities, and barrier integrity. Three members of the Ly-6/uPAR family whose functions are unknown in the cornea constitute more than 1% of the total mRNA. Aquaporin 5, epithelial membrane protein and glutathione-S-transferase (GST) omega-1, and GST alpha-4 mRNAs were preferentially expressed in distinct corneal epithelial layers, providing new markers for stratification. More than 200 tags were differentially expressed, of which 25 mediate transcription. CONCLUSIONS: In addition to providing a detailed profile of expressed genes in the PN9 and mature mouse cornea, the present SAGE data demonstrate dynamic changes in gene expression after eye opening and provide new probes for exploring corneal epithelial cell stratification, development, and function and for exploring the intricate relationship between programmed and environmentally induced gene expression in the cornea. Keywords: other
2004-01-02 | GSE887 | GEO
Project description:TAF10 interacts with the GATA1 transcription factor and controls mouse erythropoiesis
| PRJNA281703 | ENA
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility.
2014-12-04 | GSE61417 | GEO
Project description:PGCs undergo two distinct stages of demethylation before reaching a hypomethylated ground state at E13.5. Stage 1 occurs between E7.25- E9.5 in which PGCs experience a global loss of cytosine methylation. However, discreet loci escape this global loss of methylation and between E10.5-E13.5, stage 2 of demethylation takes place. In this stage these loci are targeted by Tet1 and Tet2 leading to the loss of the remaining methylation and resulting in the epigenetic ground state. Our data shows that Dnmt1 is responsible for maintaining the methylation of loci that escape stage 1 demethylation, and that it functions in a UHRF1 independent manner. Our data further demonstrates that when these loci lose methylation prior to stage 2 it results in early activation of the meiotic program, which leads to precocious differentiation of the germ line resulting in a decreased pool of PGCs in the embryo and subsequent infertility in adult mice.
2016-09-13 | GSE74938 | GEO
Project description: Not available
| S-EPMC11335981 | biostudies-literature
Project description:The acetylation levels of histones and other proteins change during aging and have been linked to neurodegeneration. Here we show that deletion of the histone acetyltransferase (HAT) co-factor Trrap specifically impairs the function of the transcription factor Sp1, reduces its stability and causes a decrease in histone acetylation at Sp1 target genes. Modulation of Sp1 function by Trrap acts as a hub regulating multiple processes involved in neuron and neural stem cells function and maintenance including microtubule dynamics and the Wnt signaling pathway. Consistently, Trrap conditional mutants exhibit all hallmarks of neurodegeneration including dendrite retraction and axonal swellings, neuron death, astrogliosis, microglia activation, demyelination and decreased adult neurogenesis. Our results uncovered a novel functional network, essential to prevent neurodegeneration, and involving the specific regulation of Sp1 transcription factor and its downstream targets by Trrap-HAT.
2021-02-17 | GSE131283 | GEO