Mesenchymal actomyosin contractility is required for androgen-driven urethral masculinization in mice
| Autor: | Kentaro Suzuki, Alvin R. Acebedo, Yuki Sato, Hisashi Haga, Gen Yamada, Robert S. Adelstein, Ken ichi Matsumoto, Naomi Nakagata, Mitsuyoshi Nakao, Toru Takeo, Shinichi Miyagawa, Shinjiro Hino, Mellissa C. Alcantara, Kenji Shimamura, Ryuichi Nishinakamura |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Male
medicine.drug_class Mesenchyme Morphogenesis Fluorescent Antibody Technique Medicine (miscellaneous) macromolecular substances Biology Models Biological Article General Biochemistry Genetics and Molecular Biology Contractility Mice Urethra MYH10 medicine Animals lcsh:QH301-705.5 Nonmuscle Myosin Type IIB Myosin Heavy Chains Mesenchymal stem cell Cell migration Actomyosin musculoskeletal system Androgen Immunohistochemistry Embryonic stem cell Cell biology medicine.anatomical_structure lcsh:Biology (General) Androgens General Agricultural and Biological Sciences Biomarkers |
| Zdroj: | Communications Biology, Vol 2, Iss 1, Pp 1-11 (2019) Communications Biology |
| ISSN: | 2399-3642 |
| DOI: | 10.1038/s42003-019-0336-3 |
| Popis: | 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. Alvin Acebedo, Kentaro Suzuki et al. show that mesenchymal-derived actomyosin contractility is required for androgen-dependent urethral masculinization in mouse embryos. They also show that actomyosin contractility regulates mesenchymal cell migration during the developmental process. |
| Databáze: | OpenAIRE |
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