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GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion [GATA3-GFP]

ABSTRACT: RNA-seq in GFP-positive and GFP-negative DN4 stage thymocytes isolated from GATA3-GFP fusion protein knock-in mouse

ORGANISM(S): Mus musculus

PROVIDER: GSE115740 | GEO | 2018/06/14

REPOSITORIES: GEO

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GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion [GATA3 overexpression]

Project description:RNA-seq in DN3a stage thymocytes isolated from wild type and GATA3 overexpression Tg mouse

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GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion [GATA3-GFP]

Project description:GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion [GATA3-GFP]

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GATA3 Abundance Is a Critical Determinant of T Cell Receptor β Allelic Exclusion.

Project description:Allelic exclusion describes the essential immunological process by which feedback repression of sequential DNA rearrangements ensures that only one autosome expresses a functional T or B cell receptor. In wild-type mammals, approximately 60% of cells have recombined the DNA of one T cell receptor β (TCRβ) V-to-DJ-joined allele in a functional configuration, while the second allele has recombined only the DJ sequences; the other 40% of cells have recombined the V to the DJ segments on both alleles, with only one of the two alleles predicting a functional TCRβ protein. Here we report that the transgenic overexpression of GATA3 leads predominantly to biallelic TCRβ gene (Tcrb) recombination. We also found that wild-type immature thymocytes can be separated into distinct populations based on intracellular GATA3 expression and that GATA3LO cells had almost exclusively recombined only one Tcrb locus (that predicted a functional receptor sequence), while GATA3HI cells had uniformly recombined both Tcrb alleles (one predicting a functional and the other predicting a nonfunctional rearrangement). These data show that GATA3 abundance regulates the recombination propensity at the Tcrb locus and provide new mechanistic insight into the historic immunological conundrum for how Tcrb allelic exclusion is mediated.

| S-EPMC5452726 | biostudies-literature

GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion [GATA3 overexpression]

Project description:GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion [GATA3 overexpression]

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GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-06-14 | GSE115745 | GEO

GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion

Project description:GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion

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Single cell- and Clumps-RNA seq from the trunk of E9.5 Pax2-GFP and Pax2-GFP Gata3 knockout embryos

Project description:Single cell- and Clumps-RNA seq from the trunk of E9.5 Pax2-GFP and Pax2-GFP Gata3 knockout embryos

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GATA3 siRNA in utricle sensory epithelia

Project description:The inner ear utilizes sensory hair cells as mechano-electric transducers for sensing sound and balance. In mammals, these hair cells lack the capacity for regeneration. Unlike mammals, hair cells from non-mammalian vertebrates, such as birds, can be regenerated throughout the life of the organism making them a useful model for studying inner ear genetics pathways. The zinc finger transcription factor GATA3 is required for inner ear development and mutations cause sensory neural deafness in humans. In the avian cochlea GATA3 is expressed throughout the sensory epithelia; however, expression is limited to the striola of the utricle. The striola corresponds to an abrupt change in morphologically distinct hair cell types and a 180Â° shift in hair cell orientation. We used 3 complimentary approaches to identify potential downstream targets of GATA3 in the avian utricle. Specifically we used microarray expression profiling of GATA3 knockdown by siRNA and GATA3 over-expression treatments as well as direct comparisons of GATA3 expressing cells from the striola and non GATA3 expressing cells from the extra-striola. Whole utricle specimens were treated with streptomycin for 24 hrs, rinsed and allowed to recover for an additional 24 hrs. Whole utricles were transfected with either GATA3 or GFP 21mer synthetic siRNAs for an additional 48 hrs and pure sensory epithelia were isolated. There are 2 biological samples and experiments include technical replicates as well as dye-switches for a total of 8 microarrays.

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Tcf1 regulates T lymphocyte lineage fidelity through its target genes Gata3 and Bcl11b

Project description:T cell factor 1 (Tcf1) is the first T cell‒specific protein induced in multipotent progenitors following Notch signaling in the thymus, leading to the activation of two major target genes, Gata3 and Bcl11b. Tcf1 deficiency results in partial arrests in T cell development high apoptosis, and increased development of B cells and myeloid cells. Phenotypically, fully T cell‒committed, Tcf1-deficient thymocytes have promiscuous gene expression, an altered epigenetic profile and can de-differentiate into more immature thymocytes and non-T cells. Expressing Bcl11b in Tcf1-deficient cells rescues T cell development, but does not strongly suppress the development of non-T cells; in contrast, expressing Gata3 suppresses the development of non-T cells, but does not rescue T cell development. Thus, T cell development is controlled by a minimal transcription factor network involving Notch signaling, Tcf1, and the subsequent division of labor between Bcl11b and Gata3, thereby ensuring a properly regulated T cell gene expression program

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Transcriptome impact of acute deletion of Gata3 in murine pro-T cells

Project description:The purpose of the study was to determine what genes in DN2 pro-T cells are immediately regulated by the transcription factor GATA-3, either as activation targets or as repression targets. To do this, two pairs of Gata3-floxed and control pro-T cells were generated and analyzed by RNA-seq within the first day of deletion of the Gata3 gene. Pro-T cells were generated by differentiation in vitro on OP9-DL1 monolayers of fetal liver-derive precursors from wildtype or Gata3-floxed mice, and the Gata3 gene was acutely deleted by transduction with Cre retroviral vector. Within 20 hr after transduction, samples of acutely Gata3-deleted and control DN2 cells were sorted and RNA prepared for RNA-seq analysis. High-throughput sequencing of the samples was carried out. Experimental Gata3 deleted samples in both cases were Gata3-floxed, ROSA26R-EYFP samples infected with Cre retrovirus and sorted for EYFP+ (Cre-activated) DN2 phenotype. Control for experiment 1: wildtype (C57BL/6) DN2 pro-T cells generated in parallel, also treated with Cre retrovirus but sorted only for DN2 phenotype. Control for experiment 2: same genotype as experimental, but infected with a GFP+ empty retroviral vector and sorted for GFP+ DN2 phenotype. Two pairs of RNA-seq samples of DN2 pro-T cells were generated for comparison, each pair consisting of a Gata3-deleted sample plus a stage-matched control.

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