ArticleCommunications biology2019
Mesenchymal actomyosin contractility is required for androgen-driven urethral masculinization in mice.
Article in Communications biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Dragon's Blood Modulates Disulfidptosis-Related Genes to Alleviate Ischemic Brain Injury in Mice.Neurochemical research · 2025Article
- Identification of disulfidptosis-related genes and subgroups in spinal cord injury.Spinal cord · 2025Article
- Characterization of urethra closure in female neonatal mice at histological and molecular levels.Reproduction (Cambridge, England) · 2024Article
- New uses for an old technique: live imaging on the slice organ culture to study reproductive processes†.Biology of reproduction · 2024Article
- An extra-genital cell population contributes to urethra closure during mouse penis development.bioRxiv : the preprint server for biology · 2023Article
- Identification of disulfidptosis-related genes and subgroups in Alzheimer's disease.Frontiers in aging neuroscience · 2023Article
- Androgen-regulatediScience · 2022Article
- One Tool for Many Jobs: Divergent and Conserved Actions of Androgen Signaling in Male Internal Reproductive Tract and External Genitalia.Frontiers in endocrinology · 2022Review
- Sexual fate of murine external genitalia development: Conserved transcriptional competency for male-biased genes in both sexes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- 3D reconstruction and histopathological analyses on murine corporal body.Reproductive medicine and biology · 2021Article
- Developmental and functional roles of androgen and interactive signals for external genitalia and erectile tissues.Reproductive medicine and biologyReview
- Emerging structural and pathological analyses on the erectile organ, corpus cavernous containing sinusoids.Reproductive medicine and biologyReview
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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