Evidence map›Paper›PMID 36175407›Full record

ArticleNature communications2022

MYPT1-PP1β phosphatase negatively regulates both chromatin landscape and co-activator recruitment for beige adipogenesis.

Hiroki Takahashi, Ge Yang, Takeshi Yoneshiro, Yohei Abe, Ryo Ito, Chaoran Yang, Junna Nakazono, Mayumi Okamoto-Katsuyama, Aoi Uchida, Makoto Arai and 24 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. 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
1.8field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

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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

34 authors at 8 institutions in 3 countries.

Hiroki Takahashi *Division of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Ge Yang *Division of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Takeshi YoneshiroDivision of Metabolic Medicine, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.ORCID 0000-0001-5298-5831
Yohei AbeDivision of Metabolic Medicine, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.ORCID 0000-0003-2519-4924
Ryo ItoDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Chaoran YangDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.ORCID 0000-0001-6639-8136
Junna NakazonoDepartment of Molecular and Cellular BioAnalysis, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, 606-8501, Japan.ORCID 0000-0001-8229-8020
Mayumi Okamoto-KatsuyamaDivision of Metabolic Medicine, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.ORCID 0000-0003-4551-7188
Aoi UchidaDivision of Metabolic Medicine, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.
Makoto AraiDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Hitomi JinDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Hyunmi ChoiDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Myagmar TumenjargalDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Shiyu XieDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Ji ZhangDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Hina SagaeDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Yanan ZhaoDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Rei YamaguchiDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Yu NomuraDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Yuichi ShimizuDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Kaito YamadaDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Satoshi YasudaDepartment of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, 980-8574, Japan.
Hiroshi KimuraCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama, 226-8503, Japan.ORCID 0000-0003-0854-083X
Toshiya TanakaDepartment of Nuclear Receptor Medicine, Laboratories for Systems Biology and Medicine, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.ORCID 0000-0003-1224-7898
Youichiro WadaIsotope Science Center, The University of Tokyo, Tokyo, 113-0032, Japan.
Tatsuhiko KodamaDepartment of Nuclear Receptor Medicine, Laboratories for Systems Biology and Medicine, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.
Hiroyuki AburataniGenome Science and Medicine Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.ORCID 0000-0003-0438-1544
Min-Sheng ZhuModel Animal Research Center and Ministry of Education (MOE) Key Laboratory of Model Animal for Disease Study, Nanjing University, 210061, Nanjing, China.ORCID 0000-0003-3256-6861
Takeshi InagakiDivision of Metabolic Medicine, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.ORCID 0000-0003-1711-8286
Timothy F OsborneInstitute for Fundamental Biomedical Research, Johns Hopkins All Children's Hospital, and Medicine in the Division of Endocrinology, Diabetes and Metabolism of the Johns Hopkins University School of Medicine, 600 Fifth Street S. St., Petersburg, FL, 33701, USA.ORCID 0000-0002-5150-4300
Takeshi KawamuraIsotope Science Center, The University of Tokyo, Tokyo, 113-0032, Japan.
Yasushi IshihamaDepartment of Molecular and Cellular BioAnalysis, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, 606-8501, Japan.ORCID 0000-0001-7714-203X
Yoshihiro MatsumuraDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan. matsumura-y@lsbm.org.ORCID 0000-0002-3108-0440
Juro SakaiDivision of Molecular Physiology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan. jmsakai@med.tohoku.ac.jp.ORCID 0000-0003-4043-1035
Tohoku University · JPThe University of Tokyo · JPKyoto University · JPGunma University · JPJohns Hopkins University · USModel Animal Research Center · CNTokyo Institute of Technology · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein kinase A promotes beige adipogenesis downstream from β-adrenergic receptor signaling by phosphorylating proteins, including histone H3 lysine 9 (H3K9) demethylase JMJD1A. To ensure homeostasis, this process needs to be reversible however, this step is not well understood. We show that myosin phosphatase target subunit 1- protein phosphatase 1β (MYPT1-PP1β) phosphatase activity is inhibited via PKA-dependent phosphorylation, which increases phosphorylated JMJD1A and beige adipogenesis. Mechanistically, MYPT1-PP1β depletion results in JMJD1A-mediated H3K9 demethylation and activation of the Ucp1 enhancer/promoter regions. Interestingly, MYPT1-PP1β also dephosphorylates myosin light chain which regulates actomyosin tension-mediated activation of YAP/TAZ which directly stimulates Ucp1 gene expression. Pre-adipocyte specific Mypt1 deficiency increases cold tolerance with higher Ucp1 levels in subcutaneous white adipose tissues compared to control mice, confirming this regulatory mechanism in vivo. Thus, we have uncovered regulatory cross-talk involved in beige adipogenesis that coordinates epigenetic regulation with direct activation of the mechano-sensitive YAP/TAZ transcriptional co-activators.

Indexed as

AdipogenesisChromatinActomyosinAnimalsCyclic AMP-Dependent Protein KinasesEpigenesis, GeneticHistonesLysineMiceMyosin-Light-Chain PhosphataseMyosin Light ChainsPhosphoric Monoester HydrolasesActomyosinChromatinCyclic AMP-Dependent Protein KinasesHistonesLysineMyosin-Light-Chain PhosphataseMyosin Light ChainsPhosphoric Monoester HydrolasesPpp1r12a protein, mouse

Identifiers

PMID36175407
PMCPMC9523048
OpenAlexW4298000113

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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.