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

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)988-994
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number4
Publication statusPublished - 03-11-2007

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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