Evidence map›Paper›PMID 29670118›Full record

ArticleNature communications2018

Global H3.3 dynamic deposition defines its bimodal role in cell fate transition.

Hai-Tong Fang, Chadi A El Farran, Qiao Rui Xing, Li-Feng Zhang, Hu Li, Bing Lim, Yuin-Han Loh

Abstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing 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

44 citing papers in PubMed.

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  7. IncRNA-ZFAS1, an Emerging Gate-Keeper in DNA Damage-Dependent Transcriptional Regulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    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

7 authors.

Hai-Tong FangEpigenetics and Cell Fates Laboratory, Programme in Stem Cell, Regenerative Medicine and Ageing, A*STAR Institute of Molecular and Cell Biology, Singapore, 138673, Singapore.
Chadi A El FarranEpigenetics and Cell Fates Laboratory, Programme in Stem Cell, Regenerative Medicine and Ageing, A*STAR Institute of Molecular and Cell Biology, Singapore, 138673, Singapore.
Qiao Rui XingEpigenetics and Cell Fates Laboratory, Programme in Stem Cell, Regenerative Medicine and Ageing, A*STAR Institute of Molecular and Cell Biology, Singapore, 138673, Singapore.
Li-Feng ZhangSchool of Biological Sciences, Nanyang Technological University, Singapore, 637551, Singapore.ORCID http://orcid.org/0000-0003-0917-0017
Hu LiCenter for Individualized Medicine, Department of Molecular Pharmacology & Experimental Therapeutics, Mayo Clinic, Rochester, MN, 55905, USA. Li.Hu@mayo.edu.ORCID http://orcid.org/0000-0001-5957-5472
Bing LimStem Cell and Regenerative Biology Group, Genome Institute of Singapore, Singapore, 138672, Singapore.
Yuin-Han LohEpigenetics and Cell Fates Laboratory, Programme in Stem Cell, Regenerative Medicine and Ageing, A*STAR Institute of Molecular and Cell Biology, Singapore, 138673, Singapore. yhloh@imcb.a-star.edu.sg.

Funding

Determinants of pancreatic cancer and malignant melanoma phenotypes in CDKN2A hereditary kindredsR01CA208517 · NCI · MAYO CLINIC ROCHESTER · PI FERNANDEZ-ZAPICO, MARTIN ERNESTO, LI, HU · 2016 to 2020
$2.9M
A network platform to connect drug response and prognosis phenotypes for cancersR01CA196631 · NCI · MAYO CLINIC ROCHESTER · PI LI, HU · 2016 to 2018
$1.2M
NCI NIH HHS R01 CA196631NCI NIH HHS R01 CA208517NIH HHS R01CA196631NIH HHS R01CA208517
6 · The paper itself

Abstract

H3.3 is a histone variant, which is deposited on genebodies and regulatory elements, by Hira, marking active transcription. Moreover, H3.3 is deposited on heterochromatin by Atrx/Daxx complex. The exact role of H3.3 in cell fate transition remains elusive. Here, we investigate the dynamic changes in the deposition of the histone variant H3.3 during cellular reprogramming. H3.3 maintains the identities of the parental cells during reprogramming as its removal at early time-point enhances the efficiency of the process. We find that H3.3 plays a similar role in transdifferentiation to hematopoietic progenitors and neuronal differentiation from embryonic stem cells. Contrastingly, H3.3 deposition on genes associated with the newly reprogrammed lineage is essential as its depletion at the later phase abolishes the process. Mechanistically, H3.3 deposition by Hira, and its K4 and K36 modifications are central to the role of H3.3 in cell fate conversion. Finally, H3.3 safeguards fibroblast lineage by regulating Mapk cascade and collagen synthesis.

Indexed as

Cell LineageAnimalsCell DifferentiationChromatin ImmunoprecipitationCollagenFibroblastsHEK293 CellsHeterochromatinHistone ChaperonesHistonesHumansMAP Kinase Signaling SystemMiceNeuronsNucleosomesPluripotent Stem CellsCollagenHeterochromatinHistone ChaperonesHistonesNucleosomes

Identifiers

PMID29670118
PMCPMC5906632

What OpenQuestion holds

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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.