Evidence map›Paper›PMID 22498630›Full record

ArticleNature2012

Genome-wide protein-DNA binding dynamics suggest a molecular clutch for transcription factor function.

Colin R Lickwar, Florian Mueller, Sean E Hanlon, James G McNally, Jason D Lieb

Abstract read
In one paragraph

Article in Nature, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed
–field-weighted citation impact
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

161 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. The next-generation sequencing-chess problem.NAR genomics and bioinformatics · 2024
    Article
  8. Article
  9. Article
  10. PML::RARA and GATA2 proteins interact via DNA templates to induce aberrant self-renewal in mouse and human hematopoietic cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Context-dependent function of the transcriptional regulator Rap1 in gene silencing and activation inProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

101 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Colin R LickwarDepartment of Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-3280, USA.
Florian Mueller
Sean E Hanlon
James G McNally
Jason D Lieb

Funding

Transcription factor mobilityZIABC010561 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MCNALLY, JAMES G · 2009 to 2013
$3.9M
Uniting disparate fields to explore transcription factor binding dynamicsR01GM072518 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LIEB, JASON D · 2005 to 2014
$2.5M
Intramural NIH HHSNIGMS NIH HHS R01 GM072518NIGMS NIH HHS R01-GM072518
6 · The paper itself

Abstract

Dynamic access to genetic information is central to organismal development and environmental response. Consequently, genomic processes must be regulated by mechanisms that alter genome function relatively rapidly. Conventional chromatin immunoprecipitation (ChIP) experiments measure transcription factor occupancy, but give no indication of kinetics and are poor predictors of transcription factor function at a given locus. To measure transcription-factor-binding dynamics across the genome, we performed competition ChIP (refs 6, 7) with a sequence-specific Saccharomyces cerevisiae transcription factor, Rap1 (ref. 8). Rap1-binding dynamics and Rap1 occupancy were only weakly correlated (R(2) = 0.14), but binding dynamics were more strongly linked to function than occupancy. Long Rap1 residence was coupled to transcriptional activation, whereas fast binding turnover, which we refer to as 'treadmilling', was linked to low transcriptional output. Thus, DNA-binding events that seem identical by conventional ChIP may have different underlying modes of interaction that lead to opposing functional outcomes. We propose that transcription factor binding turnover is a major point of regulation in determining the functional consequences of transcription factor binding, and is mediated mainly by control of competition between transcription factors and nucleosomes. Our model predicts a clutch-like mechanism that rapidly engages a treadmilling transcription factor into a stable binding state, or vice versa, to modulate transcription factor function.

Indexed as

Genome, FungalModels, BiologicalBase SequenceBinding, CompetitiveBinding SitesChromatin ImmunoprecipitationDNA, FungalGene Expression Regulation, FungalHistone AcetyltransferasesNucleosomesProtein BindingRNA, MessengerRNA Polymerase IISaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsShelterin ComplexDNA, FungalHistone AcetyltransferasesNucleosomesRAP1 protein, S cerevisiaeRNA, MessengerRNA Polymerase IISaccharomyces cerevisiae ProteinsShelterin ComplexTelomere-Binding ProteinsTranscription Factors

Identifiers

PMID22498630
PMCPMC3341663

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Registered trials

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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.