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AP-1 subunits converge promiscuously at enhancers to potentiate transcription

ABSTRACT: AP-1 subunits converge promiscuously at enhancers to potentiate transcription

PROVIDER: PRJNA641875 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12090600.fastq.gz	Fastqsanger.gz
	SRR12090601.fastq.gz	Fastqsanger.gz
	SRR12090602.fastq.gz	Fastqsanger.gz
	SRR12090603.fastq.gz	Fastqsanger.gz
	SRR12090604.fastq.gz	Fastqsanger.gz

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AP-1 subunits converge promiscuously at enhancers to potentiate transcription

Project description:The AP-1 transcription factor dimer contributes to many biological processes and environmental responses. The many ways that AP-1 subunits can dimerize has posed a challenge to understanding its regulatory function. To determine patterns of AP-1 dimerization genome-wide, we definitively establish the genome-wide binding patterns and the enhancer function of five AP-1 subunits. We find limited evidence for strong dimerization preferences between specific subunits. In particular, our analysis suggests that canonical AP-1 motifs have the potential to recruit all AP-1 subunits to genomic sites that also have hallmarks of strong enhancer activity. We term those sites AP-1 hotspots. AP-1 hotspots function as a ‘hub' for AP-1 subunit binding that elicits changes in cell-type specific AP-1-mediated gene expression. AP-1 hotspots are more predictive of genomic responses to glucocorticoid signaling than super enhancers, and are particularly enriched in disease-associated genetic variants. Together, these results support a model that promiscuous convergence of many subunits to common genomic locations potentiates AP-1-mediated transcription in a cell-type specific fashion.

2021-03-04 | GSE153254 | GEO

AP-1 subunits converge promiscuously at enhancers to potentiate transcription.

Project description:The AP-1 transcription factor (TF) dimer contributes to many biological processes and environmental responses. AP-1 can be composed of many interchangeable subunits. Unambiguously determining the binding locations of these subunits in the human genome is challenging because of variable antibody specificity and affinity. Here, we definitively establish the genome-wide binding patterns of five AP-1 subunits by using CRISPR to introduce a common antibody tag on each subunit. We find limited evidence for strong dimerization preferences between subunits at steady state and find that, under a stimulus, dimerization patterns reflect changes in the transcriptome. Further, our analysis suggests that canonical AP-1 motifs indiscriminately recruit all AP-1 subunits to genomic sites, which we term AP-1 hotspots. We find that AP-1 hotspots are predictive of cell type-specific gene expression and of genomic responses to glucocorticoid signaling (more so than super-enhancers) and are significantly enriched in disease-associated genetic variants. Together, these results support a model where promiscuous binding of many AP-1 subunits to the same genomic location play a key role in regulating cell type-specific gene expression and environmental responses.

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Mechanoresponsive genomic enhancers potentiate the cellular response to matrix stiffness

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AP-2β activates enhancers that define mammary hormone sensing cell identity [RNA-seq]

Project description:The Activating Protein 2β transcription factor (TFAP2B; AP-2β) is a marker for both lobular and molecular apocrine/HER2-E breast cancers, despite these tumours having very different prognoses. We show that simultaneous expression of both AP-2β and the estrogen receptor (ESR1, ER) marks well differentiated, low proliferation cells that are characteristic of luminal A lobular tumours, but loss of ER expression occurs when the tumour cells progress to molecular apocrine tumours. To discover potential explanations for this behaviour we performed chromatin immunoprecipitation sequencing (ChIP-seq) for AP-2β, AR, GATA3, FOXA1 and H3K27 acetylation in ER-negative MDA-MB-453 breast cancer cells. We find that all four transcription factors frequently bind to the same enhancers and that these enhancers are more likely to be active when AP-2β is present. Molecular apocrine genes are significantly more likely to have enhancers bound to all four transcription factors flanked by H3K27 acetylation. When AP-2β binds separately from the other factors, it binds close to the transcription start site, where it shows very high enrichment for H3K27 acetylation. AP-2 family proteins activate transcription by recruiting CITED proteins and p300/CBP. Since AR, FOXA1 and GATA3 are themselves able to recruit histone acetyl-transferases, we infer that AP-2β regulates the activity of those histone acetyl-transferases. We propose that this broad fundamental role in transcription explains the contradictory functions, both oncogenic and tumour suppressing, that have been assigned to AP-2 family members in previous studies on cancer.

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AP-2β activates enhancers that define mammary hormone sensing cell identity [ChIP-Seq]

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