Functional interactions between Mi-2β and AP1 complexes control response and recovery from barrier disruption
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA586885 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10381435.fastq.gz | Fastqsanger.gz | |||
| SRR10381436.fastq.gz | Fastqsanger.gz | |||
| SRR10381437.fastq.gz | Fastqsanger.gz | |||
| SRR10381438.fastq.gz | Fastqsanger.gz | |||
| SRR10381439.fastq.gz | Fastqsanger.gz |
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Project description:Keratinocytes respond to environmental signals by eliciting induction of genes that preserve skin's integrity. Here we show that the transcriptional response to stress signaling is supported by short-lived epigenetic changes. Comparison of chromatin accessibility and transcriptional changes induced by barrier disruption or by loss of the nucleosome remodeler Mi-2? identified their striking convergence in mouse and human keratinocytes. Mi-2? directly repressed genes induced by barrier disruption by restricting AP1-enriched promoter-distal sites, occupied by Mi-2? and JUNB at steady state and by c-JUN after Mi-2? depletion or stress signaling. Barrier disruption led to a modest reduction in Mi-2? expression and a further selective reduction of Mi-2? localization at stress response genes, possibly through competition with activated c-JUN. Consistent with a repressive role at stress response genes, genetic ablation of Mi-2? did not prevent reestablishment of barrier integrity but was required for return to homeostasis. Thus, a competition between Mi-2?-repressive and activating AP1 complexes may permit rapid transcriptional response to and resolution from stress signaling.
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