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A more recent version of this article appeared on September 1, 2002
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Submitted on April 9, 2002
Revised on May 16, 2002
Accepted on June 13, 2002
1 Indiana University School of Medicine, Department of Medicine, Division of Nephrology, 1120 South Drive, Fesler Hall 115, Indianapolis, IN 46202-5116
* Corresponding author. E-mail address: cphilli3{at}iupui.edu.
Nephrogenesis starts with the reciprocal induction of two embryonically distinct analages, metanephric mesenchyme and ureteric bud. This complex process requires the refined and coordinated expression of numerous developmental genes, such as inv. Mice that are homozygous for a mutation in the inv gene (inv/inv) develop renal cysts resembling autosomal-recessive polycystic kidney disease (PKD). The gene locus containing inv has been proposed to serve as a common modifier for some human and rodent PKD phenotypes. We generated polyclonal antibodies to inversin to study its subcellular distribution, potential binding partners and functional aspects in cultured murine proximal tubule cells. A 125 kD inversin protein isoform was found at cell-cell junctions. Two inversin isoforms, 140 and 90 kD, were identified in the nuclear and perinuclear compartments. Plasma membrane allocation of inversin is dependent upon cell-cell contacts and was redistributed when cell adhesion was disrupted following incubation of the cell monolayer with low-calcium/EGTA medium. We further show that the membrane-associated 125 kD inversin forms a complex with N-cadherin and the catenins. The 90 kD nuclear inversin complexes with ß-catenin. These findings indicate that the inv gene product functions in several cellular compartments including the nucleus and cell-cell adhesion sites.
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