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J Am Soc Nephrol 15:1168-1177, 2004
© 2004 American Society of Nephrology

BASIC SCIENCE

Evolutionary Conservation of Drosophila Polycystin-2 as a Calcium-Activated Cation Channel

Charles J. Venglarik, Zhiqian Gao and Xiangyi Lu

Department of Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, Alabama.

Correspondence to Dr. Charles J. Venglarik, Department of Environmental Health Sciences, University of Alabama at Birmingham, RPHB-530, 1530 3rd AVE S, Birmingham, AL 35294. Phone: 205-934-7032; Fax: 205-975-6341; E-mail: cjv{at}uab.edu

ABSTRACT. Mutations in the PKD2 gene cause autosomal dominant polycystic kidney disease (ADPKD) in humans. The protein encoded by PKD2 has similarity to voltage-sensitive cation channels and TRP channels and was named polycystin-2 (PC2). In agreement with this structural information, expression of PC2 in Xenopus oocytes or reconstitution of human PC2 in planar lipid bilayers produced Ca2+-activated cation channels. Although these studies provided a basic description of the biophysical, regulatory, and pharmacologic properties of the PC2-induced channels, it is still unknown how defective PC2 activity leads to cyst formation and expansion in ADPKD patients. To establish a genetic model for studying PC2 function and regulation, the authors identified and cloned a Drosophila PC2 (DmPC2). It is here shown that expression of DmPKD2 in Drosophila S2 cells produced a novel channel. On the basis of the similarity of this channel’s properties to mammalian PKD2-induced channels, this Drosophila channel is expected to provide a convenient genetic model for dissecting the mechanisms underlying ADPKD.




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