TY - JOUR
T1 - Loss of ICAT gene function leads to arrest of ureteric bud branching and renal agenesis
AU - Hasegawa, Yoshimi
AU - Satoh, Kiyotoshi
AU - Iizuka-Kogo, Akiko
AU - Shimomura, Atsushi
AU - Nomura, Ryuji
AU - Akiyama, Tetsu
AU - Senda, Takao
N1 - Funding Information:
We thank K. Yanagisawa, E. Kodera and K. Hikita for technical support. This study was supported by Grant-in-Aid for Scientific Research (C) 17590179 to Y.H. and Grant-in-Aid for Scientific Research (B) 16390051 to T.S. from Japan Society for the Promotion of Science, and Grants from the Fujita Health University Research Fund to Y.H. and T.S.
Copyright:
Copyright 2009 Elsevier B.V., All rights reserved.
PY - 2007/11/3
Y1 - 2007/11/3
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=34548567438&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34548567438&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2007.08.085
DO - 10.1016/j.bbrc.2007.08.085
M3 - Article
C2 - 17803964
AN - SCOPUS:34548567438
SN - 0006-291X
VL - 362
SP - 988
EP - 994
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 4
ER -