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(American Journal of Pathology. 2001;159:2347-2353.)
© 2001 American Society for Investigative Pathology

Animal Model

Failure of Ureteric Bud Invasion

A New Model of Renal Agenesis in Mice

Tomomi Kamba*{dagger}, Shin Higashi*{dagger}, Toshiyuki Kamoto{dagger}, Hayase Shisa{ddagger}, Yoshihiro Yamada*, Osamu Ogawa{dagger} and Hiroshi Hiai*

From the Departments of Pathology and Biology of Diseases*
and Urology,{dagger}
Kyoto University Graduate School of Medicine, Kyoto; and the Saitama Cancer Institute,{ddagger}
Saitama, Japan

FUBI (failure of ureteric bud invasion) is a highly inbred strain of mouse with a high spontaneous incidence of uni- or bilateral renal agenesis (60%). Bilateral renal agenesis is lethal within 2 days after birth. The primary defect of FUBI is failure of the ureteric bud to penetrate into the metanephric mesenchyme at around embryonic day 11, resulting in apoptosis of metanephric cells and leading to renal agenesis on the affected side. The metanephros seemed to be normal because co-culturing of the FUBI metanephros with homologous spinal cord induced differentiation of the rudiment, but co-culturing with the homologous ureteric bud frequently did not. Genetic analysis revealed that more than two genes were involved in this malformation and we mapped one of the modifier loci, fubi1, on chromosome 2, at ~65 cM from the centromere. In this region, there are two possible candidate genes, Wilms’ tumor 1 and formin, that play important roles in kidney development. Some of formin mutants shared a similar phenotype with FUBI; however, there was no difference in the expression of formin in embryonic kidneys between FUBI and control NFS/N mice. Studies of fubi1 congenic mice indicated that interaction of two or more loci is essential for the FUBI phenotype.






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Copyright © 2001 by the American Society for Investigative Pathology.