Polycystin-L is a calcium-regulated cation channel permeable to calcium ions

Xing-Zhen Chen, Peter M. Vassilev, Nuria Basora, Ji-Bin Peng, Hideki Nomura, Yoav Segal, Edward M. Brown, Stephen T. Reeders, Matthias A. Hediger () and Jing Zhou ()
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Xing-Zhen Chen: Renal and
Peter M. Vassilev: Brigham and Women's Hospital and Harvard Medical School
Nuria Basora: Renal and
Ji-Bin Peng: Renal and
Hideki Nomura: Renal and
Yoav Segal: Renal and
Edward M. Brown: Brigham and Women's Hospital and Harvard Medical School
Stephen T. Reeders: Renal and
Matthias A. Hediger: Renal and
Jing Zhou: Renal and

Nature, 1999, vol. 401, issue 6751, 383-386

Abstract: Abstract Polycystic kidney diseases are genetic disorders in which the renal parenchyma is progressively replaced by fluid-filled cysts1. Two members of the polycystin family (polycystin-1 and -2) are mutated in autosomal dominant polycystic kidney disease (ADPKD)2,3,4,5, and polycystin-L is deleted in mice with renal and retinal defects6. Polycystins are membrane proteins that share significant sequence homology6,7, especially polycystin-2 and -L (50% identity and 71% similarity). The functions of the polycystins remain unknown. Here we show that polycystin-L is a calcium-modulated nonselective cation channel that is permeable to sodium, potassium and calcium ions. Patch-clamp experiments revealed single-channel activity with a unitary conductance of 137 pS. Channel activity was substantially increased when either the extracellular or intracellular calcium-ion concentration was raised, indicating that polycystin-L may act as a transducer of calcium-mediated signalling in vivo. Its large single-channel conductance and regulation by calcium ions distinguish it from other structurally related cation channels.

Date: 1999
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DOI: 10.1038/43907

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