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Vol. 10, Issue 5, 659-663, May 2000

LETTER
Null Mutation of PCLN-1/Claudin-16 Results in Bovine Chronic Interstitial Nephritis

Takashi Hirano,1,3 Naohiko Kobayashi,2,3 Tomohito Itoh,1 Akiko Takasuga,1 Teruhiko Nakamaru,2 Shinji Hirotsune,1 and Yoshikazu Sugimoto1,4

1 Shirakawa Institute of Animal Genetics, Odakura, Nishigo, Nishi-shirakawa, Fukushima 961-8061, Japan; 2 Gifu Prefectural Beef Cattle Research Institute, Makigahora, Kiyomi, Gifu 506-0101, Japan

Inherited chronic renal diseases are associated with failures in glomerular filtration and tubular resorption. Such failures invariably result from defects in selective filtration and absorption in surface renal epithelium. Recently, we described an autosomal recessive chronic interstitial nephritis with diffuse zonal fibrosis (CINF) in cattle. Bovine CINF, characterized by increased blood urea nitrogen, creatinine, and urinary proteins, leads to lethality before puberty, usually within the first 6 months or year of life. Here, we demonstrate that the first four exons of PCLN-1/Claudin-16 (CL-16), which encodes a member of the claudin family of tight junction proteins, were deleted in CINF-affected cattle. CL-16 was expressed preferentially in kidneys of normal cattle, but transcripts were totally absent in affected offspring. This observation suggests that the lack of CL-16 protein contributes to the dysfunction of paracellular renal transport systems.

[The CL-16 cDNA sequence has been deposited at GenBank under accession no. AB030082.]

3 These authors contributed equally to this work.

4 Corresponding author.

10:659-663 ©2000 by Cold Spring Harbor Laboratory Press  ISSN 1088-9051/00 $5.00
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