Evidence map›Paper›PMID 16845368›Full record

ArticleEMBO reports2006

HoxB domain induction silences DNA replication origins in the locus and specifies a single origin at its boundary.

Damien Grégoire, Konstantin Brodolin, Marcel Méchali

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

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  7. Regulation of DNA replication during development.Development (Cambridge, England) · 2012
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  19. Article
  20. Programming DNA replication origins and chromosome organization.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2010
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Damien GrégoireInstitute of Human Genetics, CNRS, 141 rue de la Cardonille, 34396 Montpellier Cedex 5, France.
Konstantin Brodolin
Marcel Méchali
Centre National de la Recherche Scientifique · FRInstitut de Génétique Humaine · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In multicellular organisms, changes in the DNA replication programme could act to integrate differentiation with cell division in various developmental and transcriptional contexts. Here, we have addressed the use of DNA replication origins during differentiation in the HoxB domain-a cluster of nine genes developmentally regulated in a collinear manner. In undifferentiated mouse P19 cells, we detected several DNA replication origins in the 100 kb HoxB locus, indicating a relaxed origin use when the locus is transcriptionally silent. By contrast, in retinoic-acid-induced differentiated cells, when HoxB transcription is activated, a general silencing of DNA replication origins occurs in the locus except one located downstream of Hoxb1, at the 3' boundary of the HoxB domain. Silencing of the replication origins is associated with histone hyperacetylation, whereas the active Hoxb1 origin persists as a hypoacetylated island. These findings provide direct evidence for the differentiated use of origins in HoxB genes, and we suggest that this regulation might contribute to the regulated expression of HoxB genes during development.

Indexed as

AcetylationAnimalsCell DifferentiationCell Line, TumorChromatin ImmunoprecipitationDNA ReplicationGene Expression RegulationHistonesHomeodomain ProteinsModels, GeneticOrigin Recognition ComplexReplication OriginTranscription, GeneticTretinoinHistonesHomeodomain ProteinsOrigin Recognition ComplexTretinoin

Identifiers

PMID16845368
PMCPMC1525151
OpenAlexW2152466351

What OpenQuestion holds

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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.