Primary cilia-dependent lipid raft/caveolin dynamics regulate adipogenesis.


Journal

Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691

Informations de publication

Date de publication:
09 03 2021
Historique:
received: 15 09 2020
revised: 28 12 2020
accepted: 11 02 2021
entrez: 10 3 2021
pubmed: 11 3 2021
medline: 27 1 2022
Statut: ppublish

Résumé

Primary cilia play a pivotal role in signal transduction and development and are known to serve as signaling hubs. Recent studies have shown that primary cilium dysfunction influences adipogenesis, but the mechanisms are unclear. Here, we show that mesenchymal progenitors C3H10T1/2 depleted of trichoplein, a key regulator of cilium formation, have significantly longer cilia than control cells and fail to differentiate into adipocytes. Mechanistically, the elongated cilia prevent caveolin-1- and/or GM3-positive lipid rafts from being assembled around the ciliary base where insulin receptor proteins accumulate, thereby inhibiting the insulin-Akt signaling. We further generate trichoplein knockout mice, in which adipogenic progenitors display elongated cilia and impair the lipid raft dynamics. The knockout mice on an extended high-fat diet exhibit reduced body fat and smaller adipocytes than wild-type (WT) mice. Overall, our results suggest a role for primary cilia in regulating adipogenic signal transduction via control of the lipid raft dynamics around cilia.

Identifiants

pubmed: 33691104
pii: S2211-1247(21)00131-5
doi: 10.1016/j.celrep.2021.108817
pii:
doi:

Substances chimiques

Carrier Proteins 0
Caveolin 1 0
Igf1r protein, mouse 0
Insulin 0
RNA, Small Interfering 0
Receptor, IGF Type 1 EC 2.7.10.1
Aurka protein, mouse EC 2.7.11.1
Aurora Kinase A EC 2.7.11.1
Proto-Oncogene Proteins c-akt EC 2.7.11.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

108817

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no competing interests.

Auteurs

Daishi Yamakawa (D)

Department of Physiology, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan.

Daisuke Katoh (D)

Department of Physiology, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan; Department of Pathology and Matrix Biology, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan.

Kousuke Kasahara (K)

Department of Physiology, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan.

Takashi Shiromizu (T)

Department of Integrative Pharmacology, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan.

Makoto Matsuyama (M)

Division of Molecular Genetics, Shigei Medical Research Institute, 2117 Yamada, Minami-ku, Okayama 701-0202, Japan.

Chise Matsuda (C)

Department of Oncologic Pathology, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan.

Yumi Maeno (Y)

Department of Physiology, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan.

Masatoshi Watanabe (M)

Department of Oncologic Pathology, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan.

Yuhei Nishimura (Y)

Department of Integrative Pharmacology, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan.

Masaki Inagaki (M)

Department of Physiology, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan. Electronic address: minagaki@doc.medic.mie-u.ac.jp.

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Classifications MeSH