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Published 20 December 2004. doi:10.1083/jcb.200406025
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 167, Number 6, 1195-1204
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Article

 Roles of uroplakins in plaque formation, umbrella cell enlargement, and urinary tract diseases

Xiang-Tian Kong1, Fang-Ming Deng1,2, Ping Hu1, Feng-Xia Liang1, Ge Zhou1, Anna B. Auerbach6, Nancy Genieser3, Peter K. Nelson3, Edith S. Robbins4, Ellen Shapiro2, Bechara Kachar8, and Tung-Tien Sun1,2,5,7

1 Epithelial Biology Unit, The Ronald O. Perelman Department of Dermatology, 2 Department of Urology, 3 Department of Radiology, 4 Department of Cell Biology, 5 Department of Pharmacology, 6 Skirball Institute of Biomolecular Medicine, 7 and New York University Cancer Institute, New York University School of Medicine, New York, NY 10016
8 Section on Structural Cell Biology, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892

Correspondence to Tung-Tien Sun: sunt01{at}med.nyu.edu

The apical surface of mouse urothelium is covered by two-dimensional crystals (plaques) of uroplakin (UP) particles. To study uroplakin function, we ablated the mouse UPII gene. A comparison of the phenotypes of UPII- and UPIII-deficient mice yielded new insights into the mechanism of plaque formation and some fundamental features of urothelial differentiation. Although UPIII knockout yielded small plaques, UPII knockout abolished plaque formation, indicating that both uroplakin heterodimers (UPIa/II and UPIb/III or IIIb) are required for plaque assembly. Both knockouts had elevated UPIb gene expression, suggesting that this is a general response to defective plaque assembly. Both knockouts also had small superficial cells, suggesting that continued fusion of uroplakin-delivering vesicles with the apical surface may contribute to umbrella cell enlargement. Both knockouts experienced vesicoureteral reflux, hydronephrosis, renal dysfunction, and, in the offspring of some breeding pairs, renal failure and neonatal death. These results highlight the functional importance of uroplakins and establish uroplakin defects as a possible cause of major urinary tract anomalies and death.

X.-T. Kong, F.-M. Deng, and P. Hu contributed equally to this paper.

P. Hu's present address is Procter & Gamble Corporate Research Biotechnology, Cincinnati, OH 45252.

Abbreviations used in this paper: 2D, two-dimensional; BUN, blood urea nitrogen; ES, embryonic stem; IVP, i.v. pyelogram; UP, uroplakin; VUR, vesicoureteral reflux.


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