E-GEOD-60318
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA258019
PROVIDER: E-GEOD-60318 | ExpressionAtlas | 2015-07-29
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Two Histone/Protein Acetyltransferases, CBP and p300, Are Indispensable for Foxp3+ T-regulatory Cell Development and Function
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Project description:Regulatory T cells (Tregs) are responsible for limiting autoimmunity and chronic inflammation. Foxp3 is a transcription factor that acts as a master regulator of Treg development and function. A serendipitous observation led to the realization that a well-characterized Foxp3gfp reporter mouse, which expresses an N-terminal GFP-Foxp3 fusion protein, is a hypomorph that causes profoundly accelerated autoimmune diabetes on a NOD background. Although natural Treg development and in vitro function is not significantly altered in Foxp3gfp NOD and C57BL/6 mice, Treg fitness function in inflammatory environments is perturbed and TGF?-induced Treg development reduced. Foxp3gfpis unable to interact with the histone acetyltransferase Tip60, the histone deacetylase HDAC7, and the Ikaros family zinc finger 4, Eos, which leads to reduced Foxp3 acetylation and enhanced K48-linked polyubiquitylation. Collectively this leads to an altered transcriptional landscape and reduced Foxp3-mediated gene repression, notably at the hallmark IL-2 promoter. Loss of controlled Foxp3-driven epigenetic modification leads to Treg insufficiency that causes autoimmunity in prone environments. 16 samples overall split between 2 genotypes (wild type and Foxp3 knock in) and two cell types (Tregs and Tconv)
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Project description:Regulatory T (Treg) cells play crucial roles in suppressing deleterious immune response. Here, we investigate how mechanistically Treg cells are induced and stabilized via transcriptional regulation of Treg lineage–specifying factor Foxp3. Acetylation of histone tails in the Foxp3 locus is induced during Treg cell development and required in cis for the initiation of Foxp3 transcription. Upon induction, histone acetylation signal largely acts in trans to sustain Foxp3 transcription via multiple factors. Subsequently, Tet-mediated DNA demethylation of Foxp3 cis-regulatory elements particularly enhancer CNS2 increases chromatin accessibility and protein binding, drastically stabilizing Foxp3 transcription, although histone acetylation still regulates global gene expression. These processes transform stochastic Treg cell induction into a stable cell fate, with the former sensitive and latter resistant to genetic and environmental perturbations. Thus, our study reveals distinct roles of histone acetylation in Foxp3 induction and maintenance, reflecting sequential mechanical switches governing Treg cell lineage specification.
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Project description:Regulatory T (Treg) cells play crucial roles in suppressing deleterious immune response. Here, we investigate how mechanistically Treg cells are induced and stabilized via transcriptional regulation of Treg lineage–specifying factor Foxp3. Acetylation of histone tails in the Foxp3 locus is induced during Treg cell development and required in cis for the initiation of Foxp3 transcription. Upon induction, histone acetylation signal largely acts in trans to sustain Foxp3 transcription via multiple factors. Subsequently, Tet-mediated DNA demethylation of Foxp3 cis-regulatory elements particularly enhancer CNS2 increases chromatin accessibility and protein binding, drastically stabilizing Foxp3 transcription, although histone acetylation still regulates global gene expression. These processes transform stochastic Treg cell induction into a stable cell fate, with the former sensitive and latter resistant to genetic and environmental perturbations. Thus, our study reveals distinct roles of histone acetylation in Foxp3 induction and maintenance, reflecting sequential mechanical switches governing Treg cell lineage specification.
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