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RNA-seq and ChIP-seq to study how transcription factor Foxp1 regulates Foxp3 binding to chromatin and coordinates regulatory T cell function

ABSTRACT: RNA-seq and ChIP-seq to study how transcription factor Foxp1 regulates Foxp3 binding to chromatin and coordinates regulatory T cell function

PROVIDER: PRJNA496510 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8060920_1.fastq.gz	Fastqsanger.gz
	SRR8060920_2.fastq.gz	Fastqsanger.gz
	SRR8060930_1.fastq.gz	Fastqsanger.gz
	SRR8060930_2.fastq.gz	Fastqsanger.gz
	SRR8060940_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

RNA-seq and ChIP-seq to study how transcription factor Foxp1 regulates Foxp3 binding to chromatin and coordinates regulatory T cell function

Project description:Regulatory T (Treg) cells, whose differentiation and function are controlled by transcription factor Foxp3, express high amounts of a closely related family member Foxp1, which is also expressed in quiescent naive T cells. Here we explored Foxp1 function in Treg cells. We found that a large number of Foxp3-bound genomic sites in Treg cells were occupied by Foxp1 in both Treg and conventional T cells. In Treg cells, Foxp1 markedly increased Foxp3 binding to these sites, which were enriched for canonic forkhead and Ets binding motifs. Foxp1 deficiency in Treg cells resulted in their impaired function and competitive fitness associated with markedly reduced CD25 expression and interleukin-2 (IL-2) responsiveness, diminished CTLA-4 and increased SATB1 expression. The characteristic patterns of CD25, Foxp3, and CTLA-4 expression in Treg cells were rescued, at least in part, upon strong IL-2 signaling. Our studies suggest that in addition to the Foxp1-mediated regulation of quiescence that is common to Treg and conventional T cells, Foxp1 has an essential non-redundant function in Treg cells by enforcing Foxp3-mediated regulation of gene expression and enabling efficient IL-2 signaling in these cells.

2019-01-18 | GSE121279 | GEO

Transcription factor Foxp1 regulates Foxp3 chromatin binding and coordinates regulatory T cell function.

Project description:Regulatory T cells (Treg cells), whose differentiation and function are controlled by transcription factor Foxp3, express the closely related family member Foxp1. Here we explored Foxp1 function in Treg cells. We found that a large number of Foxp3-bound genomic sites in Treg cells were occupied by Foxp1 in both Treg cells and conventional T cells (Tconv cells). In Treg cells, Foxp1 markedly increased Foxp3 binding to these sites. Foxp1 deficiency in Treg cells resulted in their impaired function and competitive fitness, associated with markedly reduced CD25 expression and interleukin-2 (IL-2) responsiveness, diminished CTLA-4 expression and increased SATB1 expression. The characteristic expression patterns of CD25, Foxp3 and CTLA-4 in Treg cells were fully or partially rescued by strong IL-2 signaling. Our studies suggest that Foxp1 serves an essential non-redundant function in Treg cells by enforcing Foxp3-mediated regulation of gene expression and enabling efficient IL-2 signaling in these cells.

| S-EPMC7534899 | biostudies-literature

The transcription factor Foxp1 preserves integrity of an active Foxp3 locus in extrathymic Treg cells

Project description:In order to identify if there is any role of Foxp1 in the DNA demethylation of Foxp3 enhancer regions of induced Treg (iTreg) cells we performed bisulfite sequence analysis of Foxp1 deficient in vitro generated iTreg cells and compared their methylation status after 7 days of iTreg induction, at which point Foxp1 is deleted in the iTreg cells derived from Foxp3YFPCreFoxp1f/f (KO) mice.

2018-10-02 | GSE118595 | GEO

Foxp1 is critical for the maintenance of regulatory T-cell homeostasis and suppressive function

Project description:Regulatory T (Treg) cells play central roles in maintaining immune homeostasis and self-tolerance. However, the molecular mechanisms underlying Treg cell homeostasis and suppressive function are still not fully understood. Here, we report that the deletion of another P subfamily members of the forkhead box (Foxp) subfamily member Foxp1 in Treg cells led to increased numbers of activated Treg (aTreg) cells at the expense of quiescent Treg cells, and also resulted in impaired Treg suppressive function. Mice with Foxp1-deficient Treg cells developed spontaneous inflammatory disease with age; they also had more severe inflammatory disease in colitis and experimental autoimmune encephalomyelitis (EAE) models. Mechanistically, we found that Foxp1 bound to the conserved noncoding sequence 2 (CNS2) element of the Foxp3 locus and helped maintain Treg suppressive function by stabilizing the Foxp3 expression. Furthermore, we found that Foxp1 and Foxp3 coordinated the regulation of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) expression levels. Taken together, our study demonstrates that Foxp1 plays critical roles in both maintaining Treg cell quiescence during homeostasis and regulating Treg suppressive function.

2019-04-10 | GSE121251 | GEO

Elucidation of FOXP1 target genes in DLBCL by RNA-Seq

Project description:Elucidation of FOXP1 target genes by RNA-Seq of DLBCL cell lines transfected with siRNAs targeting FOXP1 expression

2015-11-30 | E-MTAB-3740 | biostudies-arrayexpress

Foxp1 developing neocortex (scATAC-Seq)

Project description:Foxp1 developing neocortex (scATAC-Seq)

| PRJNA1112381 | ENA

Foxp1 developing neocortex (snRNA-Seq)

Project description:Foxp1 developing neocortex (snRNA-Seq)

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Foxp1 developing neocortex (snRNA-Seq)

Project description:The transcription factor Foxp1 is expressed in the neocortex with restricted patterns across development. We used single nuclei-RNA sequencing (snRNA-Seq) to determine the cell-type roles of Foxp1 in control and Foxp1 conditional knock-out animals generated by crossing to Emx1.Cre hemizygous mice. Samples were collected at embyonic day (E)13.5, E16.5, and post-natal day (P)0.5.

2025-02-07 | GSE267671 | GEO

Foxp1 developing neocortex (scATAC-Seq)

Project description:The transcription factor Foxp1 is expressed in the neocortex with restricted patterns across development. We used single nuclei-ATAC sequencing (snATAC-Seq) to determine the cell-type roles of Foxp1 in control and Foxp1 conditional knock-out animals generated by crossing to Emx1.Cre hemizygous mice. Samples were collected at embyonic day (E)13.5, E16.5, and post-natal day (P)0.5.

2025-02-07 | GSE267670 | GEO

FOXP1 orchestration of ASD-relevant signaling pathways.

Project description:Mutations in the gene encoding the transcription factor forkhead box P1 or FOXP1 occur in patients with neurodevelopmental disorders, including autism. However, the function of FOXP1 in the brain remains mostly unknown. Here, we identify the gene expression program regulated by FoxP1 in both human neural cells and mouse brain and demonstrate a conserved role for FOXP1 transcriptional regulation of autism and Fragile X Mental Retardation Protein (FMRP) mediated pathways. Coexpression networks support a role for Foxp1 in neuronal activity, and we show that Foxp1 is necessary for neuronal excitability. Using a Foxp1 mouse model, we observe defects in ultrasonic vocalizations. This behavioral phenotype is reflected at the genomic level as striatal Foxp1-regulated overlap with genes known to be important in rodent vocalizations. These data support an integral role for FOXP1 in regulating signaling pathways vulnerable in developmental disorders and the specific regulation of pathways important for vocal communication. We carried out RNA-sequencing (RNA-seq) and ChIP-sequencing of human neural progenitors cells. We carried out RNA-sequencing (RNA-seq) of mouse striatal tissue, mouse hippocampal tissue and mouse cortical tissue. For the RNA-seq, four indipendent replicates were used for the neural progenitor cells and mouse tissues. For the Chip-seq, a single neural progenitor cell line was used.

2015-10-26 | E-GEOD-62718 | biostudies-arrayexpress

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