Evidence map›Paper›PMID 25922517›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

MOZ and BMI1 play opposing roles during Hox gene activation in ES cells and in body segment identity specification in vivo.

Bilal N Sheikh, Natalie L Downer, Belinda Phipson, Hannah K Vanyai, Andrew J Kueh, Davis J McCarthy, Gordon K Smyth, Tim Thomas, Anne K Voss

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

26 citing papers in PubMed, 35 citations in OpenAlex.

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  8. Tctp, a unique Ing5-binding partner, inhibits the chromatin binding of Enok inProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  14. Identification of Jmjd3 as an Essential Epigenetic Regulator ofFrontiers in cell and developmental biology · 2021
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  17. Review
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  20. Transcriptional response ofRoyal Society open science · 2017
    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

9 authors at 1 institution in 1 country.

Bilal N SheikhDevelopment and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC 3052, Australia; Department of Medical Biology, University of Melbourne, Melbourne, VIC 3052, Australia;
Natalie L DownerDevelopment and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC 3052, Australia;
Belinda PhipsonBioinformatics Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC 3052, Australia; and.
Hannah K VanyaiDevelopment and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC 3052, Australia; Department of Medical Biology, University of Melbourne, Melbourne, VIC 3052, Australia;
Andrew J KuehDevelopment and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC 3052, Australia;
Davis J McCarthyBioinformatics Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC 3052, Australia; and.
Gordon K SmythBioinformatics Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC 3052, Australia; and Department of Mathematics and Statistics, University of Melbourne, Melbourne, VIC 3052, Australia.
Tim ThomasDevelopment and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC 3052, Australia; Department of Medical Biology, University of Melbourne, Melbourne, VIC 3052, Australia; avoss@wehi.edu.au tthomas@wehi.edu.au.
Anne K VossDevelopment and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC 3052, Australia; Department of Medical Biology, University of Melbourne, Melbourne, VIC 3052, Australia; avoss@wehi.edu.au tthomas@wehi.edu.au.
Walter and Eliza Hall Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hox genes underlie the specification of body segment identity in the anterior-posterior axis. They are activated during gastrulation and undergo a dynamic shift from a transcriptionally repressed to an active chromatin state in a sequence that reflects their chromosomal location. Nevertheless, the precise role of chromatin modifying complexes during the initial activation phase remains unclear. In the current study, we examined the role of chromatin regulators during Hox gene activation. Using embryonic stem cell lines lacking the transcriptional activator MOZ and the polycomb-family repressor BMI1, we showed that MOZ and BMI1, respectively, promoted and repressed Hox genes during the shift from the transcriptionally repressed to the active state. Strikingly however, MOZ but not BMI1 was required to regulate Hox mRNA levels after the initial activation phase. To determine the interaction of MOZ and BMI1 in vivo, we interrogated their role in regulating Hox genes and body segment identity using Moz;Bmi1 double deficient mice. We found that the homeotic transformations and shifts in Hox gene expression boundaries observed in single Moz and Bmi1 mutant mice were rescued to a wild type identity in Moz;Bmi1 double knockout animals. Together, our findings establish that MOZ and BMI1 play opposing roles during the onset of Hox gene expression in the ES cell model and during body segment identity specification in vivo. We propose that chromatin-modifying complexes have a previously unappreciated role during the initiation phase of Hox gene expression, which is critical for the correct specification of body segment identity.

Indexed as

AnimalsBody PatterningEmbryo, MammalianEmbryonic Stem CellsGene Expression Regulation, DevelopmentalHistone AcetyltransferasesHomeodomain ProteinsMiceMice, Inbred BALB CMice, KnockoutPolycomb Repressive Complex 1Proto-Oncogene ProteinsBmi1 protein, mouseHistone AcetyltransferasesHomeodomain ProteinsMOZ protein, mousePolycomb Repressive Complex 1Proto-Oncogene ProteinsBMI1histone acetyltransferaselysine acetyltransferaseMYSTpolycomb

Identifiers

PMID25922517
PMCPMC4418851
OpenAlexW2040412635

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.