IRF2 ChIP seq in mouse intestinal stem cells (ISCs)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA564958 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10098846.fastq.gz | Fastqsanger.gz | |||
| SRR10098847.fastq.gz | Fastqsanger.gz | |||
| SRR11783190.fastq.gz | Fastqsanger.gz | |||
| SRR11783191.fastq.gz | Fastqsanger.gz |
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Project description:To analyze global gene-expression changes caused by IRF2 loss in ISCs, ISCs were prepared from Irf2fl/fl: Lgr5-EGFP-Ires-CreERT2(Irf2fl/fl: Lgr5ki) mice or Irf2fl/fl: Ah-Cre: Lgr5-EGFP-Ires-CreERT2 (Irf2AhcKO: Lgr5ki) mice 1 month after 5 consecutive days of βNF treatment. The Gene Ontology (GO) analysis indicated that the GO terms overrepresented among the genes upregulated in ISCs of βNF treated Irf2AhcKO: Lgr5ki mice compared with those of Irf2fl/fl: Lgr5ki mice included “immune system process”, “immune response”, and “cellular response to Interferon-beta”, all from the GOTERM_Biological Processes (BP) category. Because these GO_term inculded many IFN-inducibl genes, IFN signaling augumented in Irf2 deleted ISCs.
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Project description:Shavenbaby (Svb) transcription factor is involved in the differenciation of epidermal cells and the homeostasis of intestinal stem cells (ISCs). Svb is produced as a long repressor protein called SvbRepressor (SvbREP). In presence of Pri peptides SvbREP is processed into a shorter activator form (SvbACT) through partial proteasomal degradation of the REP domain. In ISCs, Pri triggers SvbREP to ACT maturation, while SvbREP form accumulates in differentiated enterocytes. The absence of Svb promote the apoptosis of the intestinal stem cells. In ISC, the ectopic expression of SvbREP form promote the differenciation and the SvbACT form overexpression promotes hyperplasia. (Al Hayel, et al 2020) Based on these functional analyses, Svb appears to control ISC survival and behavior, balancing proliferation and differentiation through a molecular switch between its 2 antagonistic isoforms. In this study, we determine the Svb target genes in ISCs. To this aim, we analyze the transcriptomes of ISCs upon modulation of Svb function.
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Project description:The small intestine is a rapidly proliferating organ that is maintained by a small population of Lgr5-expressing intestinal stem cells (ISCs). However, several Lgr5-negative ISC populations have been identified, and this remarkable plasticity allows the intestine to rapidly respond to both the local environment and to damage. The mediators of such plasticity are still largely unknown. Using intestinal organoids and mouse models, we show that upon ribosome impairment (driven by Rptor deletion, amino acid starvation, or low dose cyclohexamide treatment) ISCs gain an Lgr5-negative, fetal-like identity. This is accompanied by a rewiring of metabolism. Our findings suggest that the ribosome can act as a sensor of nutrient availability, allowing ISCs to respond to the local nutrient environment. Mechanistically, we show that this phenotype requires the activation of ZAKɑ, which in turn activates YAP, via SRC. Together, our data reveals a central role for ribosome dynamics in intestinal stem cells, and identify the activation of ZAKɑ as a critical mediator of stem cell identity.
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