Genome-wide chromatin occupancy of MIR205HG/LEADR in prostate basal epithelial cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA832237 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18923400.fastq.gz | Fastqsanger.gz | |||
| SRR18923401.fastq.gz | Fastqsanger.gz | |||
| SRR18923402.fastq.gz | Fastqsanger.gz | |||
| SRR18923399.fastq.gz | Fastqsanger.gz |
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Project description:Aside serving as host gene for the microRNA miR-205, MIR205HG transcribes for a nuclear chromatin-associated long noncoding RNA (lncRNA) able to restrain the differentiation of prostate basal cells, a finding that led to its reannotation as LEADR (Long Epithelial Alu-interacting Differentiation-related RNA). In our previous work (PMID: 30659180), we showed that genes that are modulated upon manipulation of MIR205HG/LEADR are characterized by the presence of an Alu sequence in their promoters. Notably, an Alu element also spans the first and second exon of MIR205HG/LEADR, thus suggesting its possible involvement in target selection and binding. Here, we performed Chromatin Isolation by RNA precipitation followed by DNA-sequencing (ChIRP-seq) to map MIR205HG/LEADR chromatin occupancy at a genome-wide level in prostate basal cells.
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Project description:Idiopathic pulmonary fibrosis (IPF) causes remodelling of distal lung, leading to respiratory failure. Pulmonary remodelling is characterised histologically not only by fibrosis but by also appearance of basal cells, yet the involvement of basal cells to IPF pathogenesis remains unclear. Here, we focus on the long non-coding RNA MIR205HG highly expressed in basal cells by single-cell RNA sequencing, to elucidate their role in IPF. Through RNA sequencing of genetic manipulations using primary cells and IPF-derived airway organoids, we uncovered MIR205HG to regulate IL33 expression. Mechanistically, the AluJb element of MIR205HG plays a key role in IL33 expression. In addition, we successfully identified a small molecule that targets this AluJb element and decreases IL33 expression. IL33 is known to induce ILC2, and MIR205HG expression positively correlated with the number of ILC2 in IPF patients. Collectively, these findings provide insights into the contributing mechanisms of basal cells to IPF and potential therapeutic targets.
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