Evidence map›Paper›PMID 28520978›Full record

ArticleNucleic acids research2017

LDB1-mediated enhancer looping can be established independent of mediator and cohesin.

Ivan Krivega, Ann Dean

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  3. Facilitators may represent a new class of regulatory elements.Current opinion in genetics & development · 2026
    Review
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  14. LDB1 establishes multi-enhancer networks to regulate gene expression.bioRxiv : the preprint server for biology · 2024
    Article
  15. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Ivan KrivegaLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Ann DeanLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

Epigenetic and Developmental Regulation of Mammalian GenesZIADK075033 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI DEAN, ANN · 2009 to 2025
$24.2M
Genomics Core FacilityZICDK071001 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2023
$16.6M
Chromatin Structure In Regulation Of Mammalian Gene ExpressionZIADK015508 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI DEAN, ANN · 2009 to 2017
$7.3M
6 · The paper itself

Abstract

Mechanistic studies in erythroid cells indicate that LDB1, as part of a GATA1/TAL1/LMO2 complex, brings erythroid-expressed genes into proximity with enhancers for transcription activation. The role of co-activators in establishing this long-range interaction is poorly understood. Here we tested the contributions of the RNA Pol II pre-initiation complex (PIC), mediator and cohesin to establishment of locus control region (LCR)/β-globin proximity. CRISPR/Cas9 editing of the β-globin promoter to eliminate the RNA Pol II PIC by deleting the TATA-box resulted in loss of transcription, but enhancer-promoter interaction was unaffected. Additional deletion of the promoter GATA1 site eliminated LDB1 complex and mediator occupancy and resulted in loss of LCR/β-globin proximity. To separate the roles of LDB1 and mediator in LCR looping, we expressed a looping-competent but transcription-activation deficient form of LDB1 in LDB1 knock down cells: LCR/β-globin proximity was restored without mediator core occupancy. Further, Cas9-directed tethering of mutant LDB1 to the β-globin promoter forced LCR loop formation in the absence of mediator or cohesin occupancy. Moreover, ENCODE data and our chromatin immunoprecipitation results indicate that cohesin is almost completely absent from validated and predicted LDB1-regulated erythroid enhancer-gene pairs. Thus, lineage specific factors largely mediate enhancer-promoter looping in erythroid cells independent of mediator and cohesin.

Indexed as

Gene Expression Regulation, LeukemicAnimalsBase Sequencebeta-GlobinsBlotting, WesternCell Cycle ProteinsCell Line, TumorChromosomal Proteins, Non-HistoneCohesinsCRISPR-Cas SystemsDNA-Binding ProteinsEnhancer Elements, GeneticLeukemia, Erythroblastic, AcuteLIM Domain ProteinsLocus Control RegionMicebeta-GlobinsCell Cycle ProteinsChromosomal Proteins, Non-HistoneCohesinsDNA-Binding ProteinsLdb1 protein, mouseLIM Domain ProteinsRNA Polymerase II

Identifiers

PMID28520978
PMCPMC5737898
OpenAlexW2614821789

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.