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AP-2α and AP-2β cooperatively orchestrate homeobox gene expression during branchial arch patterning

ABSTRACT: AP-2α and AP-2β cooperatively orchestrate homeobox gene expression during branchial arch patterning

PROVIDER: PRJNA428246 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6492321.fastq.gz	Fastqsanger.gz
	SRR6492322.fastq.gz	Fastqsanger.gz
	SRR6492323.fastq.gz	Fastqsanger.gz
	SRR6492324.fastq.gz	Fastqsanger.gz
	SRR6492325.fastq.gz	Fastqsanger.gz

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AP-2α and AP-2β cooperatively orchestrate homeobox gene expression during branchial arch patterning.

Project description:The evolution of a hinged moveable jaw with variable morphology is considered a major factor behind the successful expansion of the vertebrates. DLX homeobox transcription factors are crucial for establishing the positional code that patterns the mandible, maxilla and intervening hinge domain, but how the genes encoding these proteins are regulated remains unclear. Herein, we demonstrate that the concerted action of the AP-2α and AP-2β transcription factors within the mouse neural crest is essential for jaw patterning. In the absence of these two proteins, the hinge domain is lost and there are alterations in the size and patterning of the jaws correlating with dysregulation of homeobox gene expression, with reduced levels of Emx, Msx and Dlx paralogs accompanied by an expansion of Six1 expression. Moreover, detailed analysis of morphological features and gene expression changes indicate significant overlap with various compound Dlx gene mutants. Together, these findings reveal that the AP-2 genes have a major function in mammalian neural crest development, influencing patterning of the craniofacial skeleton via the DLX code, an effect that has implications for vertebrate facial evolution, as well as for human craniofacial disorders.

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AP-2α and AP-2β cooperatively orchestrate homeobox gene expression during branchial arch patterning

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Transcription profiling following expression of the transcription factor Hoxa2 in first branchial arch cells

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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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