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Molecular and Cellular Biology, February 2009, p. 1083-1094, Vol. 29, No. 4
0270-7306/09/$08.00+0     doi:10.1128/MCB.01163-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Deficiency of the Tetraspanin CD63 Associated with Kidney Pathology but Normal Lysosomal Function

Jenny Schröder,¹ Renate Lüllmann-Rauch,² Nina Himmerkus,³ Irina Pleines,⁴ Bernhard Nieswandt,⁴ Zane Orinska,⁵ Friedrich Koch-Nolte,⁶ Bernd Schröder,¹ Markus Bleich,³ and Paul Saftig^1*

Biochemisches Institut, Christian-Albrechts Universität Kiel, Otto-Hahn-Platz 9, D-24118 Kiel, Germany,¹ Anatomisches Institut, Christian-Albrechts Universität Kiel, Otto-Hahn-Platz 8, D-24118 Kiel, Germany,² Physiologisches Institut, Christian-Albrechts Universität Kiel, Hermann-Rodewaldstr. 5, D-24118 Kiel, Germany,³ Rudolf Virchow Center, DFG Research Center for Experimental Biomedicine, Zinklesweg 10, D-97078 Würzburg, Germany,⁴ Forschungszentrum Borstel, Abteilung Immunologie und Zellbiologie, Parkallee 22, D-23845 Borstel, Germany,⁵ Institut für Immunologie, Universitätsklinikum Eppendorf, Martinistr. 52, D-20246 Hamburg, Germany⁶

Received 23 July 2008/ Returned for modification 24 October 2008/ Accepted 2 December 2008

CD63 is a member of the tetraspanin superfamily that constitutes a main component of the lysosomal membrane. In mice, two CD63 gene loci are present, with only one of these two being functional. We generated and analyzed mice deficient for active CD63. Disruption of CD63 results in a complete loss of CD63 protein expression. Despite its abundance in late endosomes/lysosomes, the lack of CD63 does not cause obvious endosomal/lysosomal abnormalities. CD63 knockout mice are viable and fertile without gross morphological abnormalities in the majority of tissues. No alterations in the populations of immune cells and only minor differences in platelet function were observed. This suggests that the lack of CD63 could be successfully compensated for, most likely by other tetraspanins. However, CD63 deficiency leads to an altered water balance. CD63 knockout mice show an increased urinary flow, water intake, reduced urine osmolality, and a higher fecal water content. In principle cells of the collecting duct of CD63-deficient mice, abnormal intracellular lamellar inclusions were observed. This indicates that the sorting of apical transport proteins might be impaired in these cells. CD63 knockout mice provide an important tool for analyzing the various postulated functions of CD63 in vivo.

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* Corresponding author. Mailing address: Biochemisches Institut, Christian-Albrechts Universität Kiel, Otto-Hahn-Platz 9, D-24118 Kiel, Germany. Phone: 49/(0)431-8802216. Fax: 49/(0)431-8802238. E-mail: psaftig{at}biochem.uni-kiel.de

Published ahead of print on 15 December 2008.

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Molecular and Cellular Biology, February 2009, p. 1083-1094, Vol. 29, No. 4
0270-7306/09/$08.00+0     doi:10.1128/MCB.01163-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

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