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Article: JMJD3 acts in tandem with KLF4 to facilitate reprogramming to pluripotency

TitleJMJD3 acts in tandem with KLF4 to facilitate reprogramming to pluripotency
Authors
Keywordsanimal cell
animal experiment
enhancer region
female
fibroblast
Issue Date2020
PublisherNature Research (part of Springer Nature): Fully open access journals. The Journal's web site is located at http://www.nature.com/ncomms/index.html
Citation
Nature Communications, 2020, v. 11 n. 1, p. article no. 5061 How to Cite?
AbstractThe interplay between the Yamanaka factors (OCT4, SOX2, KLF4 and c-MYC) and transcriptional/epigenetic co-regulators in somatic cell reprogramming is incompletely understood. Here, we demonstrate that the histone H3 lysine 27 trimethylation (H3K27me3) demethylase JMJD3 plays conflicting roles in mouse reprogramming. On one side, JMJD3 induces the pro-senescence factor Ink4a and degrades the pluripotency regulator PHF20 in a reprogramming factor-independent manner. On the other side, JMJD3 is specifically recruited by KLF4 to reduce H3K27me3 at both enhancers and promoters of epithelial and pluripotency genes. JMJD3 also promotes enhancer-promoter looping through the cohesin loading factor NIPBL and ultimately transcriptional elongation. This competition of forces can be shifted towards improved reprogramming by using early passage fibroblasts or boosting JMJD3’s catalytic activity with vitamin C. Our work, thus, establishes a multifaceted role for JMJD3, placing it as a key partner of KLF4 and a scaffold that assists chromatin interactions and activates gene transcription.
Persistent Identifierhttp://hdl.handle.net/10722/290843
ISSN
2023 Impact Factor: 14.7
2023 SCImago Journal Rankings: 4.887
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHuang, Y-
dc.contributor.authorZhang, H-
dc.contributor.authorWang, L-
dc.contributor.authorTang, C-
dc.contributor.authorQin, X-
dc.contributor.authorWu, X-
dc.contributor.authorPan, M-
dc.contributor.authorTang, Y-
dc.contributor.authorYang, Z-
dc.contributor.authorBabarinde, IA-
dc.contributor.authorLin, R-
dc.contributor.authorJi, G-
dc.contributor.authorLai, Y-
dc.contributor.authorXu, X-
dc.contributor.authorSu, J-
dc.contributor.authorWen, X-
dc.contributor.authorSatoh, T-
dc.contributor.authorAhmed, T-
dc.contributor.authorMalik, V-
dc.contributor.authorWard, C-
dc.contributor.authorVolpe, G-
dc.contributor.authorGuo, J-
dc.contributor.authorChen, J-
dc.contributor.authorSun, L-
dc.contributor.authorL, Y-
dc.contributor.authorHuang, X-
dc.contributor.authorBao, X-
dc.contributor.authorGao, F-
dc.contributor.authorLiu, B-
dc.contributor.authorZheng, H-
dc.contributor.authorJauch, R-
dc.contributor.authorLai, L-
dc.contributor.authorPan, G-
dc.contributor.authorChen, J-
dc.contributor.authorTesta, G-
dc.contributor.authorAkira, S-
dc.contributor.authorHu, J-
dc.contributor.authorPei, D-
dc.contributor.authorHutchins, AP-
dc.contributor.authorEsteban, MA-
dc.contributor.authorQin, B-
dc.date.accessioned2020-11-02T05:47:54Z-
dc.date.available2020-11-02T05:47:54Z-
dc.date.issued2020-
dc.identifier.citationNature Communications, 2020, v. 11 n. 1, p. article no. 5061-
dc.identifier.issn2041-1723-
dc.identifier.urihttp://hdl.handle.net/10722/290843-
dc.description.abstractThe interplay between the Yamanaka factors (OCT4, SOX2, KLF4 and c-MYC) and transcriptional/epigenetic co-regulators in somatic cell reprogramming is incompletely understood. Here, we demonstrate that the histone H3 lysine 27 trimethylation (H3K27me3) demethylase JMJD3 plays conflicting roles in mouse reprogramming. On one side, JMJD3 induces the pro-senescence factor Ink4a and degrades the pluripotency regulator PHF20 in a reprogramming factor-independent manner. On the other side, JMJD3 is specifically recruited by KLF4 to reduce H3K27me3 at both enhancers and promoters of epithelial and pluripotency genes. JMJD3 also promotes enhancer-promoter looping through the cohesin loading factor NIPBL and ultimately transcriptional elongation. This competition of forces can be shifted towards improved reprogramming by using early passage fibroblasts or boosting JMJD3’s catalytic activity with vitamin C. Our work, thus, establishes a multifaceted role for JMJD3, placing it as a key partner of KLF4 and a scaffold that assists chromatin interactions and activates gene transcription.-
dc.languageeng-
dc.publisherNature Research (part of Springer Nature): Fully open access journals. The Journal's web site is located at http://www.nature.com/ncomms/index.html-
dc.relation.ispartofNature Communications-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectanimal cell-
dc.subjectanimal experiment-
dc.subjectenhancer region-
dc.subjectfemale-
dc.subjectfibroblast-
dc.titleJMJD3 acts in tandem with KLF4 to facilitate reprogramming to pluripotency-
dc.typeArticle-
dc.identifier.emailJauch, R: ralf@hku.hk-
dc.identifier.authorityJauch, R=rp02383-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/s41467-020-18900-z-
dc.identifier.pmid33033262-
dc.identifier.pmcidPMC7545202-
dc.identifier.scopuseid_2-s2.0-85092137317-
dc.identifier.hkuros318603-
dc.identifier.volume11-
dc.identifier.issue1-
dc.identifier.spagearticle no. 5061-
dc.identifier.epagearticle no. 5061-
dc.identifier.isiWOS:000581917700002-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl2041-1723-

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