Evidence map›Paper›PMID 26159997›Full record

ArticleGenes & development2015

Histone H3.3 maintains genome integrity during mammalian development.

Chuan-Wei Jang, Yoichiro Shibata, Joshua Starmer, Della Yee, Terry Magnuson

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 2 pooled it
–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

119 citing papers in PubMed, 2 syntheses or guidelines pooled it, 195 citations in OpenAlex.

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  18. Assessment of reference genes for qRT-PCR normalization to elucidate host response to African swine fever infection.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2024
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59 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Chuan-Wei JangDepartment of Genetics, Carolina Center for Genome Sciences, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599-7264, USA.
Yoichiro ShibataDepartment of Genetics, Carolina Center for Genome Sciences, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599-7264, USA.
Joshua StarmerDepartment of Genetics, Carolina Center for Genome Sciences, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599-7264, USA.
Della YeeDepartment of Genetics, Carolina Center for Genome Sciences, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599-7264, USA.
Terry MagnusonDepartment of Genetics, Carolina Center for Genome Sciences, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599-7264, USA.
University of North Carolina at Chapel Hill · USUNC Lineberger Comprehensive Cancer Center

Funding

Albino Deletion Complex and Early Mouse DevelopmentR01GM101974 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAGNUSON, TERRY R · 2012 to 2024
$5.2M
NIGMS NIH HHS R01 GM101974
6 · The paper itself

Abstract

Histone H3.3 is a highly conserved histone H3 replacement variant in metazoans and has been implicated in many important biological processes, including cell differentiation and reprogramming. Germline and somatic mutations in H3.3 genomic incorporation pathway components or in H3.3 encoding genes have been associated with human congenital diseases and cancers, respectively. However, the role of H3.3 in mammalian development remains unclear. To address this question, we generated H3.3-null mouse models through classical genetic approaches. We found that H3.3 plays an essential role in mouse development. Complete depletion of H3.3 leads to developmental retardation and early embryonic lethality. At the cellular level, H3.3 loss triggers cell cycle suppression and cell death. Surprisingly, H3.3 depletion does not dramatically disrupt gene regulation in the developing embryo. Instead, H3.3 depletion causes dysfunction of heterochromatin structures at telomeres, centromeres, and pericentromeric regions of chromosomes, leading to mitotic defects. The resulting karyotypical abnormalities and DNA damage lead to p53 pathway activation. In summary, our results reveal that an important function of H3.3 is to support chromosomal heterochromatic structures, thus maintaining genome integrity during mammalian development.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsCell DeathCell LineCell ProliferationCells, CulturedFertilityGenes, LethalGenomic InstabilityGrowth and DevelopmentHeterochromatinHistonesMiceMutationHeterochromatinHistonesapoptosiscell proliferationgenome integrityhistone H3.3mouse embryonic developmenttranscriptional regulation

Identifiers

PMID26159997
PMCPMC4511213
OpenAlexW1923705241

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.