Evidence map›Paper›PMID 34187518›Full record

ArticleGenome biology2021

Evolution of mouse circadian enhancers from transposable elements.

Julius Judd, Hayley Sanderson, Cédric Feschotte

Open access · goldAbstract read
In one paragraph

Article in Genome biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  3. PervasivebioRxiv : the preprint server for biology · 2025
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  18. Transposable Elements Co-Option in Genome Evolution and Gene Regulation.International journal of molecular sciences · 2023
    Review
  19. Article
  20. Article
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

3 authors at 2 institutions in 1 country.

Julius JuddDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY, 14853, USA.ORCID 0000-0002-4602-0205
Hayley SandersonDepartment of Human Genetics, University of Utah School of Medicine, Salt Lake City, UT, 84112, USA.
Cédric FeschotteDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY, 14853, USA. cf458@cornell.edu.ORCID 0000-0002-8772-6976
Cornell University · USUniversity of Utah · US

Funding

Genomic and Physiological Impact of Transposable Elements.R35GM122550 · NIGMS · CORNELL UNIVERSITY · PI Cedric Feschotte · 2017 to 2026
$4.4M
Connecting transposable elements and regulatory innovation using ENCODE dataU01HG009391 · NHGRI · WASHINGTON UNIVERSITY · PI COHEN, BARAK A, FESCHOTTE, CEDRIC · 2017 to 2021
$2.4M
Interrogating Enhancer Function and Cooperation by Systematic Perturbation of Transposable ElementsF31HG010820 · NHGRI · CORNELL UNIVERSITY · PI JUDD, JULIUS A. · 2019 to 2021
$107k
NHGRI NIH HHS F31 HG010820NHGRI NIH HHS U01 HG009391NIGMS NIH HHS R35 GM122550
6 · The paper itself

Abstract

backgroundTransposable elements are increasingly recognized as a source of cis-regulatory variation. Previous studies have revealed that transposons are often bound by transcription factors and some have been co-opted into functional enhancers regulating host gene expression. However, the process by which transposons mature into complex regulatory elements, like enhancers, remains poorly understood. To investigate this process, we examined the contribution of transposons to the cis-regulatory network controlling circadian gene expression in the mouse liver, a well-characterized network serving an important physiological function.

resultsChIP-seq analyses reveal that transposons and other repeats contribute ~ 14% of the binding sites for core circadian regulators (CRs) including BMAL1, CLOCK, PER1/2, and CRY1/2, in the mouse liver. RSINE1, an abundant murine-specific SINE, is the only transposon family enriched for CR binding sites across all datasets. Sequence analyses and reporter assays reveal that the circadian regulatory activity of RSINE1 stems from the presence of imperfect CR binding motifs in the ancestral RSINE1 sequence. These motifs matured into canonical motifs through point mutations after transposition. Furthermore, maturation occurred preferentially within elements inserted in the proximity of ancestral CR binding sites. RSINE1 also acquired motifs that recruit nuclear receptors known to cooperate with CRs to regulate circadian gene expression specifically in the liver.

conclusionsOur results suggest that the birth of enhancers from transposons is predicated both by the sequence of the transposon and by the cis-regulatory landscape surrounding their genomic integration site.

Indexed as

DNA Transposable ElementsEnhancer Elements, GeneticEvolution, MolecularGene Regulatory NetworksAnimalsARNTL Transcription FactorsBase SequenceBinding SitesCircadian ClocksCLOCK ProteinsCryptochromesGene Expression RegulationLiverMicePeriod Circadian ProteinsPoint MutationARNTL Transcription FactorsBmal1 protein, mouseClock protein, mouseCLOCK ProteinsCry1 protein, mouseCry2 protein, mouseCryptochromesDNA Transposable ElementsPer1 protein, mousePer2 protein, mousePeriod Circadian ProteinsTranscription FactorsCircadian rhythmsEnhancersGene regulationRegulatory evolutionTranscriptionTransposable elements

Identifiers

PMID34187518
PMCPMC8240256
OpenAlexW3175777981

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.