2023 Fiscal Year Research-status Report
Congenital reproductive tract anomalies in altered MYCN/RA axis
| Project/Area Number |
23K05601
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| Research Institution | Nagoya City University |
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Principal Investigator |
シャウキ ホッサム 名古屋市立大学, 医薬学総合研究院(医学), 助教 (70829738)
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| Co-Investigator(Kenkyū-buntansha) |
大石 久史 名古屋市立大学, 医薬学総合研究院(医学), 教授 (30375513)
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| Project Period (FY) |
2023-04-01 – 2026-03-31
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| Keywords | Wolffian duct / Anomalies / MycN |
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| Outline of Annual Research Achievements |
Congenital anomalies of the reproductive tract are common and often stem from developmental errors in the Wolffian duct in both sexes. Mutations or inhibition of retinoic acid receptors can disrupt Wolffian duct development, leading to genital malformations in males and females. Overexpression of MYCN inhibits retinoic acid signaling, potentially contributing to these anomalies. We investigated a mouse model of constitutive active MYCN (MYCN-T58M) mimicking a human patient mutation. This year, I completed the analysis of the adult mutant MYCN mouse genital tracts. The male and female mice exhibit infertility. Female mice showed imperforate vagina, uterine hydrometria, and blind-ended uterine horns, while males exhibited convoluted vas deferens and abnormal seminal vesicles. These phenomena suggest a shared congenital abnormality in reproductive tract development during embryogenesis between males and females.
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| Current Status of Research Progress |
Current Status of Research Progress
1: Research has progressed more than it was originally planned.
Reason
Half of the project has been completed
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| Strategy for Future Research Activity |
We will examine the localization of MYCN expression during embryogenesis and use histological and molecular techniques to identify the time point where the developmental abnormality started. Wolffian duct development will be deeply examined through the current project to clarify the genetic basis of reproductive tract development.
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| Causes of Carryover |
Some of the experiment planned in 2023 has been shifted to 2024.
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