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Am J Physiol Cell Physiol 280: C359-C372, 2001;
0363-6143/01 $5.00
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Vol. 280, Issue 2, C359-C372, February 2001

Differential expression of KvLQT1 and its regulator IsK in mouse epithelia

Sophie Demolombe1,*, Diego Franco1,*, Piet de Boer1, Sabina Kuperschmidt2, Dan Roden2, Yann Pereon3, Anne Jarry3, Antoon F. M. Moorman1, and Denis Escande3

1 Experimental and Molecular Cardiology Group, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; 2 Departments of Medicine, Pharmacology, Molecular Physiology & Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and 3 Laboratoire de Physiopathologie et de Pharmacologie Cellulaires et Moléculaires, Institut National de la Santé et de la Recherche Médicale U533, Hopital Hotel-Dieu, 4093 Nantes, France

KCNQ1 is the human gene responsible in most cases for the long QT syndrome, a genetic disorder characterized by anomalies in cardiac repolarization leading to arrhythmias and sudden death. KCNQ1 encodes a pore-forming K+ channel subunit termed KvLQT1 which, in association with its regulatory beta -subunit IsK (also called minK), produces the slow component of the delayed-rectifier cardiac K+ current. We used in situ hybridization to localize KvLQT1 and IsK mRNAs in various tissues from adult mice. We showed that KvLQT1 mRNA expression is widely distributed in epithelial tissues, in the absence (small intestine, lung, liver, thymus) or presence (kidney, stomach, exocrine pancreas) of its regulator IsK. In the kidney and the stomach, however, the expression patterns of KvLQT1 and IsK do not coincide. In many tissues, in situ data obtained with the IsK probe coincide with beta -galactosidase expression in IsK-deficient mice in which the bacterial lacZ gene has been substituted for the IsK coding region. Because expression of KvLQT1 in the presence or absence of its regulator generates a K+ current with different biophysical characteristics, the role of KvLQT1 in epithelial cells may vary depending on the expression of its regulator IsK. The high level of KvLQT1 expression in epithelial tissues is consistent with its potential role in K+ secretion and recycling, in maintaining the resting potential, and in regulating Cl- secretion and/or Na+ absorption.

long QT syndrome; Romano-Ward; Jervell-Lange-Nielsen; KCNQ1; KvLQT1; epithelium

* S. Demolombe and D. Franco contributed equally to this work.




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