Evidence map›Paper›PMID 30541149›Full record

ArticleNucleic acids research2019

Factor cooperation for chromosome discrimination in Drosophila.

Christian Albig, Evgeniya Tikhonova, Silke Krause, Oksana Maksimenko, Catherine Regnard, Peter B Becker

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
6.8field-weighted citation impact, top 4% 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

25 citing papers in PubMed, 48 citations in OpenAlex.

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  12. Dosage Compensation inInternational journal of molecular sciences · 2022
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  15. Dimerization Activity of a Disordered N-Terminal Domain fromInternational journal of molecular sciences · 2022
    Article
  16. Review
  17. Article
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  19. 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

6 authors at 3 institutions in 2 countries.

Christian AlbigMolecular Biology Division, Biomedical Center, Faculty of Medicine and Center for Integrated Protein Science Munich (CIPSM), Ludwig-Maximilians-Universität Munich, 82151 Martinsried, Germany.
Evgeniya TikhonovaGroup of Molecular Organization of Genome, Department of the Control of Genetic Processes, Institute of Gene Biology, Russian Academy of Sciences, 119334 Moscow, Russia.
Silke KrauseMolecular Biology Division, Biomedical Center, Faculty of Medicine and Center for Integrated Protein Science Munich (CIPSM), Ludwig-Maximilians-Universität Munich, 82151 Martinsried, Germany.
Oksana MaksimenkoGroup of Molecular Organization of Genome, Department of the Control of Genetic Processes, Institute of Gene Biology, Russian Academy of Sciences, 119334 Moscow, Russia.
Catherine RegnardMolecular Biology Division, Biomedical Center, Faculty of Medicine and Center for Integrated Protein Science Munich (CIPSM), Ludwig-Maximilians-Universität Munich, 82151 Martinsried, Germany.
Peter B BeckerMolecular Biology Division, Biomedical Center, Faculty of Medicine and Center for Integrated Protein Science Munich (CIPSM), Ludwig-Maximilians-Universität Munich, 82151 Martinsried, Germany.
Center for Integrated Protein Science Munich · DEInstitute of Gene Biology · RULudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcription regulators select their genomic binding sites from a large pool of similar, non-functional sequences. Although general principles that allow such discrimination are known, the complexity of DNA elements often precludes a prediction of functional sites. The process of dosage compensation in Drosophila allows exploring the rules underlying binding site selectivity. The male-specific-lethal (MSL) Dosage Compensation Complex (DCC) selectively binds to some 300 X chromosomal 'High Affinity Sites' (HAS) containing GA-rich 'MSL recognition elements' (MREs), but disregards thousands of other MRE sequences in the genome. The DNA-binding subunit MSL2 alone identifies a subset of MREs, but fails to recognize most MREs within HAS. The 'Chromatin-linked adaptor for MSL proteins' (CLAMP) also interacts with many MREs genome-wide and promotes DCC binding to HAS. Using genome-wide DNA-immunoprecipitation we describe extensive cooperativity between both factors, depending on the nature of the binding sites. These are explained by physical interaction between MSL2 and CLAMP. In vivo, both factors cooperate to compete with nucleosome formation at HAS. The male-specific MSL2 thus synergises with a ubiquitous GA-repeat binding protein for refined X/autosome discrimination.

Indexed as

Dosage Compensation, GeneticAnimalsBinding SitesChromatinChromosomesDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsGene Expression RegulationGenome, InsectNuclear ProteinsNucleosomesProtein BindingTranscription FactorsX ChromosomeChromatinCLAMP protein, DrosophilaDNA-Binding ProteinsDrosophila Proteinsmsl-2 protein, DrosophilaNuclear ProteinsNucleosomesTranscription Factors

Identifiers

PMID30541149
PMCPMC6393291
OpenAlexW2949147174

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.