Transcriptome analysis of WEHI B lymphoma cells overexpressing individual NFATc1 proteins
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB13854 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1397910.fastq.gz | Fastqsanger.gz | |||
| ERR1397901.fastq.gz | Fastqsanger.gz | |||
| ERR1397911.fastq.gz | Fastqsanger.gz | |||
| ERR1397902.fastq.gz | Fastqsanger.gz | |||
| ERR1397912.fastq.gz | Fastqsanger.gz |
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Project description:In lymphocytes, NFATc1 is the most prominent NFAT transcription factor which play a crucial role in the fate and activity of peripheral T and B cells. NFATc1 is synthesized in two prominent isoforms, the inducible short isoform NFATc1/aA and the constitutively expressed long isoform NFATc1/C. Several lines of evidence suggested that both isoforms differ markedly in their function. It was speculated that NFATc1/aA supports the proliferation and survival of lymphocytes, whereas NFATc1/C should support apoptosis and anergy induction. To proof this hypothesis we established WEHI 231 B lymphoma cells that stably (over-) express either NFATc1/aA or NFATc1/C. In preliminary experiments we could should that WEHI cells overexpressing NFATc1/aA were protected against apoptosis induction, while cells overexpressing NFATc1/C should a higher apoptosis rate. Transcriptom analysis of WEHI-231 cells overexpressing either NFATc1/aA or NFATc1/C were performed, along with a control group of WEHI-231 cells overexpressing the E.coli enzyme BirA Ligase (which is also present in all target cell lines since for further molecular assays the NFATc1 proteins were expressed as chimeric protein containing C-terminal bio-tags. The experimental results obtained indicate that the both NFATc1 proteins, NFATc1/aA and NFATc1/C, differ tremendously in their transcriptional properties.
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Project description:Post-translational modification with SUMO is known to regulate the activity of transcription factors, but how SUMOylation of individual proteins might influence immunity is mostly unexplored. The NFAT transcription factors play an essential role in antigen receptor-mediated gene regulation. SUMOylation of NFATc1 represses IL-2 in vitro, but its role in T cell-mediated immune responses in vivo is not clear. To this end, we generated a novel Nfatc1 transgenic mouse, which prevents SUMO modification of NFATc1. Avoidance of NFATc1 SUMOylation ameliorated experimental autoimmune encephalomyelitis as well as graft-versus-host disease. An elevated IL-2 production promoted Treg expansion and suppressed autoreactive or alloreactive T cells. Mechanistically, increased IL-2 secretion counteracted IL-17 and IFN-γ expression through STAT5 and Blimp-1 induction. Then, Blimp-1 repressed IL-2 itself and the as well induced, proliferation-associated survival factor Bcl2A1. Collectively, we demonstrate that prevention of NFATc1 SUMOylation fine-tunes T-cell responses towards lasting tolerance. Thus, targeting NFATc1 SUMOylation presents a novel and promising strategy to treat T cell-mediated inflammatory diseases.
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Project description:Post-translational modification with SUMO is known to regulate the activity of transcription factors, but how SUMOylation of individual proteins might influence immunity is mostly unexplored. NFATc1 is a transcription factor of the family of ‘Nuclear Factors of Activated T-cells’ which plays an essential role in antigen receptor-mediated gene regulation. It is expressed in multiple isoforms of which the longer isoforms can be modified by SUMOylation. SUMO modification of NFATc1 represses IL-2 in vitro, but its role in T cell-mediated immune responses in vivo is not clear. To this end, we generated a novel Nfatc1 transgenic mouse with lysine to arginine mutations, which abolish the SUMO modification within NFATc1’s C-terminal domain. Inhibition of NFATc1 SUMOylation ameliorated experimental autoimmune encephalomyelitis as well as graft-versus-host disease. This was due to elevated IL-2 production that promoted Treg expansion and suppressed autoreactive or alloreactive T cells. Mechanistically, increased IL-2 secretion counteracted IL-17 and IFN-γ expression through STAT5 and Blimp-1 induction. Blimp-1 also repressed IL-2 itself and the as well induced survival factor Bcl2A1. Still, lack of NFATc1 sumoylation fine-tunes T-cell responses towards lasting tolerance implying a novel approach to treat inflammatory diseases.
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Project description:We performed the newly mapping of genome-wide NFATc1 binding events in VEGF-stimulated primary cultured endothelial cells, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). Combined NFATc1 ChIP-seq profile and the epigenetic histone marks revealed that predominant NFATc1-occupied peaks were overlapped with promoter marking but not silencer marking. DNA microarrays with NFATc1 expression or knockdown indicated the predominant NFATc1 binding targets were correlated with induced patterns. To determine NFATc1-regulated genes, a total of 5 samples were derived from human umbilical vein endothelial cells (HUVECs) stimulated with or without 50ng/mL VEGF (VEGF 60min and 0min, respectively), pretreated with cyclosporine A (VEGF 60min plus CsA) and infected with adenovirus expressing the control or constitutively active NFATc1 (Ad-control and Ad-NFATc1).
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Project description:Genetic deletion of Nfatc1 in mice results in profound osteoclast-poor osteopetrosis, a high bone mass state caused by a lack of osteoclast activity. We hypothesized that the family of NFATc1 regulated transcripts in the osteoclast would be enriched for genes associated with osteoclast function. We used microarrays profile gene expression in wild-type and NFATc1-deficient osteoclasts generated in vitro to identify NFATc1-dependent transcripts in osteoclasts. Bone marrow macrophages from wild-type and mice with an induced deficiency of NFATc1 (NFATc1 fl/fl MxCre+ mice where NFATc1 excision was induced by polyIC treatment) were cultured ex vivo in MCSF and RANKL for 3 days. 2 biological replicates were assayed for each genotype.
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Project description:We find that epithelial-specific deletion of Nfatc1 decreases skin tumor susceptibility in mice subjected to DMBA/TPA carcinogenesis. To probe the molecular mechanisms by which Nfatc1 may regulate tumorigenesis, we identify gene expression changes associated with constitutive NFATc1 activation in primary mouse keratinocytes. Constitutively active NFATc1 activity in primary mouse keratinocytes to investigate how Nfatc1 regulates tumor initiation in the skin.
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Project description:We performed the newly mapping of genome-wide NFATc1 binding events in VEGF-stimulated primary cultured endothelial cells, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). Combined NFATc1 ChIP-seq profile and the epigenetic histone marks revealed that predominant NFATc1-occupied peaks were overlapped with promoter marking but not silencer marking. DNA microarrays with NFATc1 expression or knockdown indicated the predominant NFATc1 binding targets were correlated with induced patterns.
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Project description:We performed the newly mapping of genome-wide NFATc1 binding events in VEGF-stimulated primary cultured endothelial cells, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). Combined NFATc1 ChIP-seq profile and the epigenetic histone marks revealed that predominant NFATc1-occupied peaks were overlapped with promoter marking but not silencer marking. DNA microarrays with NFATc1 expression or knockdown indicated the predominant NFATc1 binding targets were correlated with induced patterns. Examination of NFATc1 and two different histone marks in HUVEC in the presence/absense of VEGF.
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