Abstract
Wnt/β-catenin signalling regulates numerous developmental and homeostatic processes. Ctnnb1 (also known as β-catenin) is the only protein that transmits signals from various Wnt ligands to downstream genes. In this study, we report that our newly established mouse strain, which harbours a Cys429 to Ser missense mutation in the β-catenin gene, exhibited specific organ defects in contrast to mice with broadly functioning Wnt/β-catenin signalling. Both homozygous mutant males and females produced normal gametes but were infertile because of abnormal seminal vesicle and vaginal morphogenesis. An ins-TOPGAL transgenic reporter spatiotemporally sustained Wnt/β-catenin signalling during the corresponding organogenesis. Therefore, β-cateninC429S should provide new insights into β-catenin as a universal component of Wnt/β-catenin signal transduction.
Highlights
Wnt/b-catenin signalling regulates numerous developmental and homeostatic processes
The ins-TOPGAL transgenic reporter[5] visualized abnormally sustained Wnt/b-catenin signalling during organogenesis of the seminal vesicle and vagina in homozygous mutant males and females, respectively
Unlike the previously reported conditional knockout mice, b-cateninC429S mice, which lack Cre drivers and express b-catenin via the endogenous promoter, exhibited a unique pattern of infertility resulting from specific defects in the organogenesis of the seminal vesicle (Fig. 1) and vagina (Fig. 2), the sperm and oocytes were normal (Table S3)
Summary
Correspondence and requests for materials should be addressed to T.M. (takuya_m@brc. riken.jp) b-cateninC429S mice exhibit sterility consequent to spatiotemporally sustained Wnt signalling in the internal genitalia. We report that our newly established mouse strain, which harbours a Cys[429] to Ser missense mutation in the b-catenin gene, exhibited specific organ defects in contrast to mice with broadly functioning Wnt/b-catenin signalling Both homozygous mutant males and females produced normal gametes but were infertile because of abnormal seminal vesicle and vaginal morphogenesis. The ins-TOPGAL transgenic reporter[5] visualized abnormally sustained Wnt/b-catenin signalling during organogenesis of the seminal vesicle and vagina in homozygous mutant males and females, respectively. As shown in the previous report[12], we observed normal Wnt/bcatenin signalling activity in the wild-type seminal vesicle and vagina In the homozygous mutants, sustained Wnt/b-catenin signalling was spatiotemporally limited to the very caudal Wolffian ducts of both sexes during organogenesis (Fig. S5)
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