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Loss of Zfp335 triggers cGAS/STING-dependent apoptosis of post-B-selection pre-T cells [scRNA-seq]

ABSTRACT: The transcription factor Zfp335 is esstential for the survival of post-B-selection DN4 thymocytes. We utilized 10x Genomics v3 platform to profile the transcriptomes of

ORGANISM(S): Mus musculus

PROVIDER: GSE189243 | GEO | 2022/09/13

REPOSITORIES: GEO

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Loss of Zfp335 triggers cGAS/STING-dependent apoptosis of post-B-selection pre-T cells [TCRa-seq]

Project description:The transcription factor Zfp335 is esstential for the survival of post-B-selection DN4 thymocytes. We utilized TCRa repertoire sequencing to assess alterations to survival duration for Zfp335-deficient DP thymocytes.

2022-09-13 | GSE205323 | GEO

Loss of Zfp335 triggers cGAS/STING-dependent apoptosis of post-B-selection pre-T cells [RNA-seq]

Project description:The transcription factor Zfp335 is esstential for the survival of post-B-selection DN4 thymocytes. We utilized RNA-seq to profile the alterations to the transcriptional profiles of Zfp335-deficient DP thymocytes

2022-09-13 | GSE189242 | GEO

Zinc finger protein Zfp335 controls thymocyte differentiation and survival through b-selection-dependent and -independent mechanisms

Project description:T cell development proceeds in a series of developmental stages, which is precisely orchestrated by multiple signaling and molecular networks. Here we found a zinc finger protein Zfp335 intrinsically controls DN to DP transition, as T cell-specific deficiency in Zfp335 leads to a substantial accumulation of DN3 along with reduction of DP, CD4+ and CD8+ thymocytes. This developmental blockade at DN stage results from the impaired intracellular TCRβ expression as well as increased susceptibility to apoptosis in thymocytes. Transcriptomic and ChIP-seq analyses revealed a direct regulation of transcription factors Bcl6 and Rorc by Zfp335. Importantly, enhanced expression of TCRβ and Bcl6/RorγT restores the developmental defect during DN3 to DN4 transition and improves thymocytes survival, respectively. These findings identify a critical role of Zfp335 in controlling T cell development by maintaining intracellular TCR expression-mediated β-selection and independently activating cell survival signaling.

2021-12-30 | GSE184532 | GEO

Zinc finger protein Zfp335 controls thymocyte differentiation and survival through b-selection-dependent and -independent mechanisms [ChIP-seq]

2021-12-30 | GSE184705 | GEO

Loss of Zfp335 triggers cGAS/STING-dependent apoptosis of post-B-selection pre-T cells

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

2022-09-13 | GSE189244 | GEO

Genome-wide profiling of Zfp335 binding sites in thymocytes

Project description:The generation of naM-CM-/ve T lymphocytes is critical for immune function yet the mechanisms governing their maturation remain incompletely understood. We have identified a mouse mutant, bloto, that harbors a hypomorphic mutation in the zinc finger protein Zfp335. Mutant blt/blt mice exhibit a naM-CM-/ve T cell deficiency due to an intrinsic developmental defect that begins to manifest in the thymus and continues into the periphery, affecting T cells that have recently undergone thymic egress. Zfp335 binds to promoter regions via a consensus motif, and its target genes are enriched in categories related to protein metabolism, mitochondrial function and transcriptional regulation. Restoring the expression of one target, Ankle2, partially rescues T cell maturation. Our findings identify Zfp335 as a transcription factor and essential regulator of late-stage intrathymic and post-thymic T cell maturation. 4 Zfp335 ChIP-seq samples and 2 input samples with WT vs. blt/blt thymocytes.

2014-10-17 | E-GEOD-58333 | biostudies-arrayexpress

Gene expression profiling of mature CD4 SP thymocytes from a mouse strain with an ENU-induced mutation in Zfp335

Project description:The generation of naM-CM-/ve T lymphocytes is critical for immune function yet the mechanisms governing their maturation remain incompletely understood. We have identified a mouse mutant, bloto, that harbors a hypomorphic mutation in the zinc finger protein Zfp335. Mutant blt/blt mice exhibit a naM-CM-/ve T cell deficiency due to an intrinsic developmental defect that begins to manifest in the thymus and continues into the periphery, affecting T cells that have recently undergone thymic egress. Zfp335 binds to promoter regions via a consensus motif, and its target genes are enriched in categories related to protein metabolism, mitochondrial function and transcriptional regulation. Restoring the expression of one target, Ankle2, partially rescues T cell maturation. Our findings identify Zfp335 as a transcription factor and essential regulator of late-stage intrathymic and post-thymic T cell maturation. WT and blt/blt mature CD4SP thymocytes were sorted from mixed hematopoietic chimeras for RNA extraction and gene expression analysis on Affymetrix arrays. 6 samples were analyzed in total, with 3 biological replicates per genotype.

2014-10-17 | E-GEOD-58288 | biostudies-arrayexpress

Zfp335 establishes neonatal immune tolerance through safeguarding effector Treg lineage commitment and maintenance [ChIP-seq]

Project description:Regulatory T (Treg) cells are crucial for maintaining peripheral immune tolerance and preventing destructive autoreactive responses, but how heterogeneous Treg populations establish tolerant status remains unclear. Here, we found that Zinc finger protein 335 (Zfp335) is indispensable for the differentiation and maintenance of effector Treg (eTreg) population and immunological self-tolerance in neonates. Mice with Zfp335 deletion in Treg cells exhibit early-onset autoimmune disease with severe inflammation in multiple organs and unrestricted activation and expansion of conventional T cells. Zfp335-deficient Treg cells display dysfunctional and pathogenic features together with multiple defects in proliferation, survival and suppressive function. Importantly, our single-cell RNA sequencing (scRNA-seq) analyses reveal distinct Treg populations and that Zfp335 deficiency causes an almost complete loss of eTreg population along with significant accumulation of dysfunctional Treg populations. Mechanistically, Zfp335 controls both fate decision and homeostasis of eTreg cells by directly targeting genes associated with homeostasis and oxidation-fueled oxidative phosphorylation (OXPHOS) and PI3K-Akt-mTOR metabolic pathways. Our data establish the concept that Zfp335 serves as a checkpoint and safeguard for eTreg lineage commitment and maintenance.

2022-02-28 | GSE189076 | GEO

Genome-wide profiling of Zfp335 binding sites in thymocytes

Project description:The generation of naïve T lymphocytes is critical for immune function yet the mechanisms governing their maturation remain incompletely understood. We have identified a mouse mutant, bloto, that harbors a hypomorphic mutation in the zinc finger protein Zfp335. Mutant blt/blt mice exhibit a naïve T cell deficiency due to an intrinsic developmental defect that begins to manifest in the thymus and continues into the periphery, affecting T cells that have recently undergone thymic egress. Zfp335 binds to promoter regions via a consensus motif, and its target genes are enriched in categories related to protein metabolism, mitochondrial function and transcriptional regulation. Restoring the expression of one target, Ankle2, partially rescues T cell maturation. Our findings identify Zfp335 as a transcription factor and essential regulator of late-stage intrathymic and post-thymic T cell maturation.

2014-10-17 | GSE58333 | GEO

Interleukin-7 co-ordinates proliferation, differentiation and TCRA recombination during thymocyte β-selection

Project description:We used Illumina global gene expression profiling to compare IL7-regulated pathways in post-beta-selected DN3b and DN4 versus pre-beta-selected DN3a cell stages. We found that IL7 induced fewer genes in both DN3b and DN4 cells (800 and 300 respectively, versus 1800 in DN3a). We found several direct JAK/STAT target genes were significantly induced in all 3 stages. This group included Bcl2 and Cish, Socs2 and Socs3, feedback regulators of JAK-STAT signaling, as well as Pim1, Tfrc (Cd71) and Ccnd2. Thus, in addition to inducing survival genes, here we show that IL7 acutely regulates expression of trophic receptors and cell cycle regulators in pre- and post-beta-selection DN thymocytes.

2015-02-05 | GSE63932 | GEO

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