Loss of ICAT gene function leads to arrest of ureteric bud branching and renal agenesis

Yoshimi Hasegawa, Kiyotoshi Satoh, Akiko Iizuka-Kogo, Atsushi Shimomura, Ryuji Nomura, Tetsu Akiyama, Takao Senda

研究成果: Article査読

7 被引用数 (Scopus)

抄録

ICAT, inhibitor of β-catenin and T cell factor, or Ctnnbip1, is a negative regulator of the Wnt signaling pathway that interferes with the interaction between β-catenin and T cell factor. Some ICAT-deficient (ICAT-/-) embryos exhibit unilateral or bilateral renal agenesis. In this study, we investigated developmental processes in the ICAT-/- kidney. ICAT was highly expressed in both the ureteric bud (UB) and the surrounding metanephric mesenchymal (MM) cells in the metanephros of embryonic day E11.5-E13.5 wild-type (ICAT+/+) mouse. In the E12.5-ICAT-/- metanephros, UB branching was delayed, and a T-shaped, bifurcated UB was frequently seen; this was never seen in the E12.5-ICAT+/+ metanephros. More apoptotic MM cells were detected in the ICAT-/- metanephros than in the ICAT+/+ metanephros. These results suggest that the loss of ICAT gene function causes the arrest of UB branching and the apoptotic death of MM cells, resulting in renal agenesis.

本文言語English
ページ(範囲)988-994
ページ数7
ジャーナルBiochemical and Biophysical Research Communications
362
4
DOI
出版ステータスPublished - 03-11-2007

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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