Ligand dependent gene regulation by transient ERα clustered enhancers

Unliganded Estrogen receptor alpha (ERα) has been implicated in ligand-dependent gene regulation. Upon ligand exposure, ERα binds to several EREs relatively proximal to the pre-marked, unliganded ERα-bound sites and affects transient but robust gene expression. However, the underlying mechanisms are...

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Published in:PLoS genetics 2020-01, Vol.16 (1), p.e1008516
Main Authors: Saravanan, Bharath, Soota, Deepanshu, Islam, Zubairul, Majumdar, Sudeshna, Mann, Rajat, Meel, Sweety, Farooq, Umer, Walavalkar, Kaivalya, Gayen, Srimonta, Singh, Anurag Kumar, Hannenhalli, Sridhar, Notani, Dimple
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Language:English
Subjects:
Biology and Life Sciences
Chromatin
Chromatin Assembly and Disassembly
Condensates
CRISPR
Enhancer Elements, Genetic
Enhancers
Estrogen Receptor alpha - genetics
Estrogen Receptor alpha - metabolism
Gene Deletion
Gene expression
Gene regulation
Genomes
Genomics
Histones - metabolism
Humans
Ligands
MCF-7 Cells
Trefoil Factor-1 - genetics
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creator Saravanan, Bharath
Soota, Deepanshu
Islam, Zubairul
Majumdar, Sudeshna
Mann, Rajat
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Farooq, Umer
Walavalkar, Kaivalya
Gayen, Srimonta
Singh, Anurag Kumar
Hannenhalli, Sridhar
Notani, Dimple
description Unliganded Estrogen receptor alpha (ERα) has been implicated in ligand-dependent gene regulation. Upon ligand exposure, ERα binds to several EREs relatively proximal to the pre-marked, unliganded ERα-bound sites and affects transient but robust gene expression. However, the underlying mechanisms are not fully understood. Here we demonstrate that upon ligand stimulation, persistent sites interact extensively, via chromatin looping, with the proximal transiently ERα-bound sites, forming Ligand Dependent ERα Enhancer Cluster in 3D (LDEC). The E2-target genes are regulated by these clustered enhancers but not by the H3K27Ac super-enhancers. Further, CRISPR-based deletion of TFF1 persistent site disrupts the formation of its LDEC resulting in the loss of E2-dependent expression of TFF1 and its neighboring genes within the same TAD. The LDEC overlap with nuclear ERα condensates that coalesce in a ligand and persistent site dependent manner. Furthermore, formation of clustered enhancers, as well as condensates, coincide with the active phase of signaling and their later disappearance results in the loss of gene expression even though persistent sites remain bound by ERα. Our results establish, at TFF1 and NRIP1 locus, a direct link between ERα condensates, ERα enhancer clusters, and transient, but robust, gene expression in a ligand-dependent fashion.
doi_str_mv 10.1371/journal.pgen.1008516
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subjects Biology and Life Sciences
Chromatin
Chromatin Assembly and Disassembly
Condensates
CRISPR
Enhancer Elements, Genetic
Enhancers
Estrogen Receptor alpha - genetics
Estrogen Receptor alpha - metabolism
Gene Deletion
Gene expression
Gene regulation
Genomes
Genomics
Histones - metabolism
Humans
Ligands
MCF-7 Cells
Trefoil Factor-1 - genetics
title Ligand dependent gene regulation by transient ERα clustered enhancers
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