Unknown,Transcriptomics,Genomics,Proteomics

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Transient ER binding and p300 redistribution support a physiological squelching model for immediate ER-repressed genes

ABSTRACT: Selective transcriptional activation and repression of genes throughout signaling cascades and development are poorly understood. Transcription factors (TF) orchestrate patterns and magnitude of transcriptional response, but TF action, or inaction, is highly dependent upon TF kinetics, distance from genes, chromatin architecture, and the local occupancy of other TFs. We integrated genomic transcription, chromosome looping, TF binding, and chromatin structure data to analyze the molecular cascade that results from estradiol-induced (E2) signaling in human MCF-7 breast cancer cells and addressed the context-specific nature of gene regulation. We analyzed kinetic ChIP-seq that profiled the master regulator of the E2-mediated response, estrogen receptor (ER), and found that transient ER binding sites are specifically associated with enhancers of repressed genes. We performed replicate ChIP-seq experiments prior to estrogen treatment and 2min, 5min, 10min, 40min, and 160min after E2 treatment.

ORGANISM(S): Homo sapiens

SUBMITTER: Michael Guertin 

PROVIDER: E-GEOD-54855 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transient estrogen receptor binding and p300 redistribution support a squelching mechanism for estradiol-repressed genes.

Guertin Michael J MJ   Zhang Xuesen X   Coonrod Scott A SA   Hager Gordon L GL  

Molecular endocrinology (Baltimore, Md.) 20140722 9

Proper gene regulation is essential for proper organismal development and appropriate responses to external stimuli. Specialized factors, termed master regulators, are often responsible for orchestrating the molecular events that result from signaling cascades. Master regulators coordinate the activation and repression of specific gene classes. Estrogen receptor α (ER) precipitates the signaling cascade that results from endogenous or exogenous estrogen hormones. ER is a classic transcriptional  ...[more]

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