Evidence map›Paper›PMID 38729154›Full record

ArticleStem cell reports2024

Reduction of H3K9 methylation by G9a inhibitors improves the development of mouse SCNT embryos.

Shogo Matoba, Daiki Shikata, Fumiyuki Shirai, Takaki Tatebe, Michiko Hirose, Akiko Nakata, Naomi Watanabe, Ayumi Hasegawa, Akihiro Ito, Minoru Yoshida and 1 more

Abstract read
In one paragraph

Article in Stem cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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

11 authors.

Shogo MatobaBioresource Engineering Division, Bioresource Research Center, RIKEN, Tsukuba, Ibaraki 305-0074, Japan; Cooperative Division of Veterinary Sciences, Tokyo University of Agriculture and Technology, Fuchu, Tokyo 183-8509, Japan. Electronic address: shogo.matoba@riken.jp.
Daiki ShikataBioresource Engineering Division, Bioresource Research Center, RIKEN, Tsukuba, Ibaraki 305-0074, Japan; Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8572, Japan.
Fumiyuki ShiraiDrug Discovery Chemistry Platform Unit, RIKEN Center for Sustainable Resource Science, Wako, Saitama 351-0198, Japan.
Takaki TatebeBioresource Engineering Division, Bioresource Research Center, RIKEN, Tsukuba, Ibaraki 305-0074, Japan; Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8572, Japan.
Michiko HiroseBioresource Engineering Division, Bioresource Research Center, RIKEN, Tsukuba, Ibaraki 305-0074, Japan.
Akiko NakataDrug Discovery Seed Compounds Exploratory Unit, RIKEN Center for Sustainable Resource Science, Wako, Saitama 351-0198, Japan.
Naomi WatanabeBioresource Engineering Division, Bioresource Research Center, RIKEN, Tsukuba, Ibaraki 305-0074, Japan; Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8572, Japan.
Ayumi HasegawaBioresource Engineering Division, Bioresource Research Center, RIKEN, Tsukuba, Ibaraki 305-0074, Japan.
Akihiro ItoLaboratory of Cell Signaling, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo 192-0392, Japan; Chemical Genomics Research Group, RIKEN Center for Sustainable Resource Science, Wako, Saitama 351-0198, Japan.
Minoru YoshidaDrug Discovery Seed Compounds Exploratory Unit, RIKEN Center for Sustainable Resource Science, Wako, Saitama 351-0198, Japan; Chemical Genomics Research Group, RIKEN Center for Sustainable Resource Science, Wako, Saitama 351-0198, Japan; Office of University Professors, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan.
Atsuo OguraBioresource Engineering Division, Bioresource Research Center, RIKEN, Tsukuba, Ibaraki 305-0074, Japan; Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8572, Japan; The Center for Disease Biology and Integrative Medicine, Faculty of Medicine, University of Tokyo, Tokyo 113-0033, Japan; Bioresource Engineering Laboratory, RIKEN Cluster for Pioneering Research, Wako, Saitama 351-0198, Japan. Electronic address: atsuo.ogura@riken.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Removal of somatic histone H3 lysine 9 trimethylation (H3K9me3) from the embryonic genome can improve the efficiency of mammalian cloning using somatic cell nuclear transfer (SCNT). However, this strategy involves the injection of histone demethylase mRNA into embryos, which is limiting because of its invasive and labor-consuming nature. Here, we report that treatment with an inhibitor of G9a (G9ai), the major histone methyltransferase that introduces H3K9me1/2 in mammals, greatly improved the development of mouse SCNT embryos. Intriguingly, G9ai caused an immediate reduction of H3K9me1/2, a secondary loss of H3K9me3 in SCNT embryos, and increased the birth rate of cloned pups about 5-fold (up to 3.9%). G9ai combined with the histone deacetylase inhibitor trichostatin A further improved this rate to 14.5%. Mechanistically, G9ai and TSA synergistically enhanced H3K9me3 demethylation and boosted zygotic genome activation. Thus, we established an easy, highly effective SCNT protocol that would enhance future cloning research and applications.

Indexed as

Histone-Lysine N-MethyltransferaseHistonesNuclear Transfer TechniquesAnimalsCloning, OrganismEmbryo, MammalianEmbryonic DevelopmentFemaleHistone Deacetylase InhibitorsHydroxamic AcidsMethylationMiceG9a protein, mouseHistone Deacetylase InhibitorsHistone-Lysine N-MethyltransferaseHistonesHydroxamic Acidstrichostatin AcloningG9aH3K9me3H3K9 methylationinhibitorKdm3amouseRK-701Somatic cell nuclear transfertrichostatin A

Identifiers

PMID38729154
PMCPMC11390627

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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.