International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


POSTER 78 - FAILURE OF URETERIC BUD INVASION: A NEW MODEL OF RENAL AGENESIS IN MICE

Dr Tomomi Kamba
Kyoto University
Yoshida-Konoe-cho, Sakyo-ku
Kyoto 606-8501
Japan

Co-Authors: 1)Higashi S, 1)Kamoto T, 2)Shisa H, 3)Yamada Y, 1)Ogawa O, 3)Hiai H
Institutions: 1)Department of Urology, Kyoto University Graduate School of Medicine 2) Saitma Cancer Institute, 3)Department of Pathology and Biology of Pathology and Biology of Diseases, Kyoto University Graduate School of Medicine

FUBI (Failure of Ureteric Bud Invasion) is a highly inbred strain of mouse with a high spontaneous incidence of unilateral 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 apotosis of metanephric cells and leading to renal agenesis on the affected side. The metanephros seemed to be normal because coculturing of the FUBI metanephros with homologous spinal cord induced differentiation of the rudiment, but coculturing 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 about 65cM from the centromere. In this region, there are two possible candidate genes, Wilms tumour 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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