| 研究実績の概要 |
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.
|
