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Global gene-regulatory targets of FOSL1, FOSL2 and BATF in human Th17 cells [RNA-seq]

ABSTRACT: The aim of this study was to investigate the transciptional mechanisms governed by FOSL1, FOSL2 and BATF for regulation of human Th17 cell-function. FOSL factors were transiently perturbed using RNAi (KD) and over-expression (OE) strategies, whereas BATF was perturbed using RNAi only. RNA-seq was then performed to determine their global transciptional targets.

ORGANISM(S): Homo sapiens

PROVIDER: GSE174809 | GEO | 2022/04/12

REPOSITORIES: GEO

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Genome-wide binding sites of FOSL1, FOSL2 and BATF in human Th17 cells [ChIP-seq]

Project description:The aim of this study was to investigate the transciptional mechanisms governed by FOSL1, FOSL2 and BATF for regulation of human Th17 cell-function. To determine the genome-wide binding sites of these factors, ChIP-seq analysis was performed using in vitro derived Th17 cells at 72h of polarization.

2022-04-12 | GSE174810 | GEO

Mapping interactome networks of FOSL1 and FOSL2 in human Th17 cells

Project description:The differentiation of Th17 cells is controlled by a complex network of transcription factors (TFs), including FOS and JUN proteins of the AP-1 family. The FOS-like proteins, FOSL1 and FOSL2 have recently been reported to control Th17 responses. The molecular mechanisms dictating their roles, however, are unclear. Moreover, although the functions of AP-1 TFs are largely governed by their protein-protein interactions, these are also poorly characterized in this milieu. Using affinity purification in combination with mass-spectrometry we established the first interactomes of FOSL1 and FOSL2 in human Th17 cells. In addition to their known interactions with JUN proteins, our analysis identified several novel binding partners of FOSL factors. Gene ontology analysis revealed RNA binding was enriched as the major functionality for FOSL1 and FOSL2 associated proteins, thereby suggesting possible mechanistic links that have not been studied before. Intriguingly, 29 interactors were found to be shared between FOSL1 and FOSL2, which included crucial regulators of Th17-fate. These findings, including unique and shared interactions, were validated using parallel reaction monitoring targeted mass-spectrometry (PRM-MS), with additional measurements with other laboratory methods. Overall, this study provides key insights into interaction-based signalling mechanisms of FOSL1 and FOSL2, which potentially control Th17 cell-development and associated pathologies.

2021-11-02 | PXD025729 | Pride

Genome-wide binding sites of FOSL1, FOSL2 and BATF in human Th17 cells [ChIP-seq]

Project description:Genome-wide binding sites of FOSL1, FOSL2 and BATF in human Th17 cells [ChIP-seq]

| PRJNA731664 | ENA

Global gene-regulatory targets of FOSL1, FOSL2 and BATF in human Th17 cells [RNA-seq]

Project description:Global gene-regulatory targets of FOSL1, FOSL2 and BATF in human Th17 cells [RNA-seq]

| PRJNA731665 | ENA

Global gene-regulatory targets and Genome-wide binding sites of FOSL1, FOSL2 and BATF in human Th17 cells

Project description:Global gene-regulatory targets and Genome-wide binding sites of FOSL1, FOSL2 and BATF in human Th17 cells

| PRJNA734773 | ENA

A systematic comparison of FOSL1, FOSL2 and BATF-mediated transcriptional regulation during early human Th17 differentiation.

Project description:Th17 cells are essential for protection against extracellular pathogens, but their aberrant activity can cause autoimmunity. Molecular mechanisms that dictate Th17 cell-differentiation have been extensively studied using mouse models. However, species-specific differences underscore the need to validate these findings in human. Here, we characterized the human-specific roles of three AP-1 transcription factors, FOSL1, FOSL2 and BATF, during early stages of Th17 differentiation. Our results demonstrate that FOSL1 and FOSL2 co-repress Th17 fate-specification, whereas BATF promotes the Th17 lineage. Strikingly, FOSL1 was found to play different roles in human and mouse. Genome-wide binding analysis indicated that FOSL1, FOSL2 and BATF share occupancy over regulatory regions of genes involved in Th17 lineage commitment. These AP-1 factors also share their protein interacting partners, which suggests mechanisms for their functional interplay. Our study further reveals that the genomic binding sites of FOSL1, FOSL2 and BATF harbour hundreds of autoimmune disease-linked SNPs. We show that many of these SNPs alter the ability of these transcription factors to bind DNA. Our findings thus provide critical insights into AP-1-mediated regulation of human Th17-fate and associated pathologies.

| S-EPMC9122603 | biostudies-literature

Transcription profiling by array of mouse M1 cells expressing Batf targeting siRNA or control siRNA and treated with leukemia inhibitory factor to identify putative downstream targets of Batf

Project description:In order to identify putative downstream targets of Batf in M1 cells, a microarray analysis was performed. Briefly, M1/Neg-RNAi (expressing control siRNA with no mammalian target) and M1/Batf-RNAi cells (expressing Batf targeting siRNA) were seeded in M1 growth medium at a density of 3 X 105/ml in 100mm culture dishes. Six plates were plated for each cell type. Within each group, three were labeled as + LIF and treated with leukemia inhibitory factor (LIF) (5 ng/ml) for 6 hours the following day. After 6 hours, the cells were harvested from all plates individually and RNA prepared. 5 µg of total RNA from the three individual samples representing each subgroup (M1/Neg-RNAi + LIF, - LIF; M1/Batf-RNAi + LIF, - LIF) were combined into one pool of RNA. EJT001 represents sample "M1/Neg-RNAi, no LIF)"; EJT002 represents sample "M1/Neg-RNAi, with LIF)"; EJT003 represents sample "M1/Batf-RNAi, no LIF)"; EJT004 represents sample "M1/Batf-RNAi, with LIF)". The four pools of RNA were shipped to Genome Explorations, Inc. for analysis using Affymetrix GeneChip technology. The differentially regulated genes were identified both within each group (+ LIF compared to - LIF) and between 2 goups (M1/Neg-RNAi and M1/Batf-RNAi).

2011-03-01 | E-MEXP-2995 | biostudies-arrayexpress

Mapping interactome networks of FOSL1 and FOSL2 in human Th17 cells

2021-09-18 | PXD025840 | panorama

ChIP-seq analysis of MED1 and FOSL1 in SCC1 cells after depletion of FOSL1

Project description:To explore genome-wide alteration MED1 and FOSL1 after depletion of FOSL1, we performed chromatin immunoprecipitation sequencing (ChIP-seq) of SCC1 cells to examine genome-wide recruitment of MED1 and FOSL1 following FOSL1 knockdown. Depletion of FOSL1 led to dramatically loss of the recruitment of MED1 and FOSL1 at a cohort of key oncogenes associate with tumorigenesis and metastasis.

2021-04-14 | GSE151132 | GEO

Interactome Networks of FOSL1 and FOSL2 in Human Th17 Cells.

Project description:Dysregulated function of Th17 cells has implications in immunodeficiencies and autoimmune disorders. Th17 cell differentiation is orchestrated by a complex network of transcription factors, including several members of the activator protein (AP-1) family. Among the latter, FOSL1 and FOSL2 modulate the effector functions of Th17 cells. However, the molecular mechanisms underlying these effects are unclear, owing to the poorly characterized protein interaction networks of FOSL factors. Here, we establish the first interactomes of FOSL1 and FOSL2 in human Th17 cells, using affinity purification-mass spectrometry analysis. In addition to the known JUN proteins, we identified several novel binding partners of FOSL1 and FOSL2. Gene ontology analysis found a significant fraction of these interactors to be associated with RNA-binding activity, which suggests new mechanistic links. Intriguingly, 29 proteins were found to share interactions with FOSL1 and FOSL2, and these included key regulators of Th17 fate. We further validated the binding partners identified in this study by using parallel reaction monitoring targeted mass spectrometry and other methods. Our study provides key insights into the interaction-based signaling mechanisms of FOSL proteins that potentially govern Th17 cell differentiation and associated pathologies.

| S-EPMC8482465 | biostudies-literature

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