Mesenchymal actomyosin contractility is required for androgen-driven urethral masculinization in mice.


Journal

Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179

Informations de publication

Date de publication:
2019
Historique:
received: 30 08 2018
accepted: 01 02 2019
entrez: 20 3 2019
pubmed: 20 3 2019
medline: 20 3 2019
Statut: epublish

Résumé

The morphogenesis of mammalian embryonic external genitalia (eExG) shows dynamic differences between males and females. In genotypic males, eExG are masculinized in response to androgen signaling. Disruption of this process can give rise to multiple male reproductive organ defects. Currently, mechanisms of androgen-driven sexually dimorphic organogenesis are still unclear. We show here that mesenchymal-derived actomyosin contractility, by MYH10, is essential for the masculinization of mouse eExG. MYH10 is expressed prominently in the bilateral mesenchyme of male eExG. Androgen induces MYH10 protein expression and actomyosin contractility in the bilateral mesenchyme. Inhibition of actomyosin contractility through blebbistatin treatment and mesenchymal genetic deletion induced defective urethral masculinization with reduced mesenchymal condensation. We also suggest that actomyosin contractility regulates androgen-dependent mesenchymal directional cell migration to form the condensation in the bilateral mesenchyme leading to changes in urethral plate shape to accomplish urethral masculinization. Thus, mesenchymal-derived actomyosin contractility is indispensable for androgen-driven urethral masculinization.

Identifiants

pubmed: 30886905
doi: 10.1038/s42003-019-0336-3
pii: 336
pmc: PMC6408527
doi:

Substances chimiques

Androgens 0
Biomarkers 0
Actomyosin 9013-26-7
Nonmuscle Myosin Type IIB EC 3.6.1.-
nonmuscle myosin type IIB heavy chain EC 3.6.1.-
Myosin Heavy Chains EC 3.6.4.1

Types de publication

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

Langues

eng

Pagination

95

Déclaration de conflit d'intérêts

The authors declare no competing interests.

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Auteurs

Alvin R Acebedo (AR)

1Department of Developmental Genetics, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, 641-8509 Japan.

Kentaro Suzuki (K)

1Department of Developmental Genetics, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, 641-8509 Japan.

Shinjiro Hino (S)

2Department of Medical Cell Biology, Institute of Molecular Embryology and Genetics (IMEG), Kumamoto University, Kumamoto, 860-0811 Japan.

Mellissa C Alcantara (MC)

1Department of Developmental Genetics, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, 641-8509 Japan.

Yuki Sato (Y)

3Department of Anatomy and Cell Biology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582 Japan.

Hisashi Haga (H)

4Transdisciplinary Life Science Course, Faculty of Advanced Life Science, Hokkaido University, N10-W8, Kita-ku, Sapporo, 060-0810 Japan.

Ken-Ichi Matsumoto (KI)

5Department of Biosignaling and Radioisotope Experiment, Interdisciplinary Center for Science Research, Organization for Research, Shimane University, Izumo, Shimane, 693-8501 Japan.

Mitsuyoshi Nakao (M)

2Department of Medical Cell Biology, Institute of Molecular Embryology and Genetics (IMEG), Kumamoto University, Kumamoto, 860-0811 Japan.

Kenji Shimamura (K)

6Department of Brain Morphogenesis, Institute of Molecular Embryology and Genetics (IMEG), Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto, 860-0811 Japan.

Toru Takeo (T)

7Division of Reproductive Engineering, Center for Animal Resources and Development (CARD), Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto, 860-0811 Japan.

Naomi Nakagata (N)

7Division of Reproductive Engineering, Center for Animal Resources and Development (CARD), Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto, 860-0811 Japan.

Shinichi Miyagawa (S)

1Department of Developmental Genetics, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, 641-8509 Japan.

Ryuichi Nishinakamura (R)

8Department of Kidney Development, Institute of Molecular Embryology and Genetics (IMEG), Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto, 860-0811 Japan.

Robert S Adelstein (RS)

9Laboratory of Molecular Cardiology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1762 USA.

Gen Yamada (G)

1Department of Developmental Genetics, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, 641-8509 Japan.

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Classifications MeSH