Region-specific DNA-binding properties of NFIA in the adult mouse brain
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ABSTRACT:
PROVIDER: PRJNA609158 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11195145_1.fastq.gz | Fastqsanger.gz | |||
| SRR11195145_2.fastq.gz | Fastqsanger.gz | |||
| SRR11195146_1.fastq.gz | Fastqsanger.gz | |||
| SRR11195146_2.fastq.gz | Fastqsanger.gz | |||
| SRR11195147_1.fastq.gz | Fastqsanger.gz |
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Project description:The goal of this study is to profile NFIA DNA-binding properties in the adult mouse brain. We performed chromatin immunoprecipitation of NFIA in the hippocampus and olfactory bulb of wildtype mice, and samples were subjected to sequencing. We find that NFIA preferentially binds DNA in the hippocampus but not in the olfactory bulb as evidenced by the distinct lack of NFIA binding peaks in the olfactory bulb. Mass spectrometry results suggested that NFIA has a significantly higher binding affinity for NFIB in the olfactory bulb, potentially blocking NFIA’s ability to bind DNA. Virally induced siRNAs against NFIB or scramble were injected into the olfactory bulb of adult wildtype mice to knock down NFIB. We performed chromatin immunoprecipitation of NFIA in the olfactory bulb injected with siRNA-NFIB or siRNA-scramble. Subsequent sequencing revealed an increase of NFIA binding in the olfactory bulb upon the depletion of NFIB as compared to the siRNA-scramble and wildtype controls.
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Project description:Since the NFI transcription factors have been shown to be key regulators of gliogenesis, we utilized this pathway to identify miRNAs involved in the regulation of the neurogenesis-to-gliogenesis switch by neural stem/progenitor cells (NSPCs). We focused on miRNAs with expression levels that were differentially regulated downstream of NFIA, and established a mouse embryonic stem cell (ESC) line that expresses NFIA in a doxycycline (Dox)-dependent manner. NFIA-overexpressing (OE) and control NSPCs (neurospheres) derived from ESCs were purified from their mixed cultures (primary neursphsres (PNs) or secondary neurospheres (SNs) ) by fluorescence activated cell sorting and subjected to miRNAarray analysis.
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Project description:Since the NFI transcription factors have been shown to be key regulators of gliogenesis, we utilized this pathway to identify miRNAs involved in the regulation of the neurogenesis-to-gliogenesis switch by neural stem/progenitor cells (NSPCs). We focused on miRNAs with expression levels that were differentially regulated downstream of NFIA, and established a mouse embryonic stem cell (ESC) line that expresses NFIA in a doxycycline (Dox)-dependent manner. NFIA-overexpressing (OE) and control NSPCs (neurospheres) derived from ESCs were purified from their mixed cultures (primary neursphsres (PNs) or secondary neurospheres (SNs) ) by fluorescence activated cell sorting and subjected to the gene expression microrray analysis.
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Project description:The NFIA-ETO2 fusion is the product of a t(1;16)(p31;q24) chromosomal translocation so far exclusively found in pediatric patients with pure erythroid leukemia (PEL). To address its role for the pathogenesis of the pure erythroid leukemia, we retrovirally expressed the PEL-associated NFIA-ETO2 fusion in MEL cells. To better identify direct target gene loci, we sequenced NFIA-ETO2-associated immunoprecipitated chromatin and histone modifications.
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Project description:Regional gene expression profiling upon loss of NFIA in adult astrocytes
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Project description:Adipose tissue is central to regulation of systemic energy homeostasis. Adaptive thermogenesis in brown and beige adipocytes, which relies on mitochondrial oxidative phosphorylation, dissipates energy to counteract obesity. On the other hand, chronic inflammation in adipose tissue is linked to insulin resistance, type 2 diabetes and obesity. Here we show that nuclear factor I-A (NFIA), a transcriptional regulator of brown and beige adipocytes, improves systemic glucose homeostasis via up-regulation of oxidative phosphorylation and reciprocal down-regulation of inflammation. Mice with transgenic expression of NFIA in adipocytes exhibited improved glucose tolerance, increased energy expenditure and limited weight gain on high fat diet. NFIA coordinately up-regulate genes involved in oxidative phosphorylation as well as a battery of brown-fat-specific genes through enhancer activation that involves facilitated genomic binding of PPARγ. In contrast, NFIA in adipocytes, but not in macrophages, down-regulate pro-inflammatory cytokine genes to ameliorate adipose tissue inflammation in vivo. NFIA binds to enhancer/promoter region of Ccl2 gene that encodes pro-inflammatory cytokine MCP-1, to down-regulate its transcription. NFIA expression and CCL2 expression was negatively correlated in human adipose tissue. These results indicate that NFIA in adipocytes reciprocally regulate mitochondrial and inflammatory gene program to improve systemic glucose homeostasis.
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