The role of RPA1 in T cell
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA783417 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17035395.fastq.gz | Fastqsanger.gz | |||
| SRR17035396.fastq.gz | Fastqsanger.gz |
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Project description:As a single strand DNA binding protein, RPA1 participates various cellular processes including DNA replication and DNA repair.However, the role of RPA1 in T cell is largely unknown. We generate a mice model in which RPA1 was specifically deleted in T cell. Through single cell RNA sequencing, we reveal the immune landscape in RPA1 conditional knockout mice.
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Project description:Replication protein A1 (RPA1) is a single-stranded DNA binding protein that is known to participate in DNA replication, recombination and damage repair. However, little is known about RPA1’s role in controlling chromatin architecture and gene transcription. Further, physiological functions of RPA1 in mouse tissues still remain exclusive. Here we show that Rpa1 heterozygous mice developed age-depended fatty liver disease and are more susceptible to hepatic steatosis in response to high-fat diet. Liver specific deletion of Rpa1 impairs fatty acid oxidation, leading to hepatic steatosis and high incidence of hepatocellular carcinoma. Transcriptome analysis identified down-regulation of fatty acid oxidation related genes. Cleavage Under Targets and Tagmentation (CUT&Tag) and Assay for transposase-accessible chromatin using sequencing (ATAC-seq) revealed that RPA1 binds and regulates chromatin accessibility in regulatory regions of a group of genes involved in lipid metabolism in liver. Further, down-regulation of RPA1 was found in patients with fatty liver disease. Thus, our results not only established that RPA1 is critical controller of chromatin architecture and regulator of gene transcription, but also provided new insights into the epigenetic mechanism of fatty liver disease, which could inform future therapy.
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Project description:The peripheral T cell pool is maintained at dynamic homeostasis throughout life. This is achieved through fine-tuning of thymic output and self-renewal of naïve T cells. Dysregulation of T cell homeostasis has been implicated in autoimmune diseases, yet little is known about the homeostatic mechanisms. Here, we report that the replication protein A1 (RPA1) is upregulated during T cell activation. Utilizing T cell-specific Rpa1-deficient (Rpa1fl/fl Cd4-cre) mice, we find that loss of Rpa1 restrains peripheral CD8+ T cell population and limits TCR repertoire diversity. Clinical analysis reveals that the mRNA level of RPA1 is reduced in patients with ulcerative colitis. Accordingly, Rpa1fl/fl Cd4-cre mice exhibit increased susceptibility to inflammatory diseases, including colitis and hepatitis. Mechanistically, RPA1 deficiency triggers necroptotic T cell death following TCR engagement, which in turn results in damage-associated molecular patterns (DAMPs) leakage and leukocyte recruitment, consequently exacerbating inflammatory damage. These studies thus uncover that RPA1 acts as a guardian of T cell clonal expansion that is essential for T cell homeostasis.
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