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The phosphorylation of FOXA1-S331 is indispensable for FOXA1-AR dependent cistrome [RNA-seq]

ABSTRACT: The phosphorylation of FOXA1-S331 is indispensable for FOXA1-AR dependent cistrome [RNA-seq]

PROVIDER: PRJNA971091 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24490389_1.fastq.gz	Fastqsanger.gz
	SRR24490389_2.fastq.gz	Fastqsanger.gz
	SRR24490390_1.fastq.gz	Fastqsanger.gz
	SRR24490390_2.fastq.gz	Fastqsanger.gz
	SRR24490391_1.fastq.gz	Fastqsanger.gz

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The phosphorylation of FOXA1-S331 is indispensable for FOXA1-AR dependent cistrome.

Project description:The phosphorylation of FOXA1-S331 is indispensable for FOXA1-AR dependent cistrome.

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The phosphorylation of FOXA1-S331 is indispensable for FOXA1-AR dependent cistrome [RNA-seq]

Project description:To define the function of FOXA1-S331 phosphorylation, we substituted S331 in both FOXA1 alleles for alanine in C4-2 cells via CRISPR/Cas9-based gene editing, thereby generating phosphorylation incompetent FOXA1S331A cells. We directly assessed the consequences of phospho-incompetent FOXA1S331A mutation on the transcription profile, chromatin deposition of FOXA1, AR, H3K27ac and chromatin accessibility.

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The phosphorylation of FOXA1-S331 is indispensable for FOXA1-AR dependent cistrome [Cut&Tag]

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The phosphorylation of FOXA1-S331 is indispensable for FOXA1-AR dependent cistrome [Cut&Tag]

Project description:The phosphorylation of FOXA1-S331 is indispensable for FOXA1-AR dependent cistrome [Cut&Tag]

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The phosphorylation of FOXA1-S331 is indispensable for FOXA1-AR dependent cistrome [ATAC-seq]

Project description:The phosphorylation of FOXA1-S331 is indispensable for FOXA1-AR dependent cistrome [ATAC-seq]

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Pioneer factor FOXA1 defines GATA2- and AR-mediated transcriptional program in prostate cancer [ChIP-Seq]

Project description:AR is tightly regulated by many transcriptional cofactors, including key pioneer factor such as FOXA1 and GATA2. While FOXA1 was recently shown to be able to redistribute AR across the genome, how GATA2 regulates AR cistrome has not been carefully investigated. Here, we report that, unlike FOXA1, GATA2 is unable to reprogram AR, but instead it enhances AR program by inducing AR expression and augmenting AR co-occupancy, thereby acting as a pure AR coactivator, rather than a pioneer factor. On the other hand, AR co-occupancy enhances both GATA2 and FOXA1 binding on the chromatin, forming a positive feedback loop. Importantly, we found that FOXA1 is also capable of reprogramming GATA2 by recruiting GATA2 from GATA motif to FKHD-containing regions, being analogous to its pioneering effect on AR signaling. By contrast, GATA2 simply acts as a co-activator of FOXA1 with a lack of pioneering ability. ChIP_Seq examination of AR, FoxA1 and GATA2 binding sites in LNCaP and DU145 cells

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