Kcnq 1-5 (Kv7.1-5) potassium channel expression in the adult zebrafish

Calvin Wu,Christina Torres,Kyle Laster,Thomas J Lukas,Kanishk Sharma,Ernest J Moore,Mohamed Hersi

doi:10.1186/1472-6793-14-1

Abstract

BackgroundKCNQx genes encode slowly activating-inactivating K+ channels, are linked to physiological signal transduction pathways, and mutations in them underlie diseases such as long QT syndrome (KCNQ1), epilepsy in adults (KCNQ2/3), benign familial neonatal convulsions in children (KCNQ3), and hearing loss or tinnitus in humans (KCNQ4, but not KCNQ5). Identification of kcnqx potassium channel transcripts in zebrafish (Danio rerio) remains to be fully characterized although some genes have been mapped to the genome. Using zebrafish genome resources as the source of putative kcnq sequences, we investigated the expression of kcnq1-5 in heart, brain and ear tissues.ResultsOverall expression of the kcnqx channel transcripts is similar to that found in mammals. We found that kcnq1 expression was highest in the heart, and also present in the ear and brain. kcnq2 was lowest in the heart, while kcnq3 was highly expressed in the brain, heart and ear. kcnq5 expression was highest in the ear. We analyzed zebrafish genomic clones containing putative kcnq4 sequences to identify transcripts and protein for this highly conserved member of the Kcnq channel family. The zebrafish appears to have two kcnq4 genes that produce distinct mRNA species in brain, ear, and heart tissues.ConclusionsWe conclude that the zebrafish is an attractive model for the study of the KCNQ (Kv7) superfamily of genes, and are important to processes involved in neuronal excitability, cardiac anomalies, epileptic seizures, and hearing loss or tinnitus.

Highlights

KCNQx genes encode slowly activating-inactivating K+ channels, are linked to physiological signal transduction pathways, and mutations in them underlie diseases such as long QT syndrome (KCNQ1), epilepsy in adults (KCNQ2/3), benign familial neonatal convulsions in children (KCNQ3), and hearing loss or tinnitus in humans (KCNQ4, but not KCNQ5)
Of the several ion channels used by the sensory hair cell, the K+ channel KCNQ4 is thought to modulate the membrane potential of hair cells to adjust the sensitivity of hearing in a variety of mammals [1,4,5]
A recent study characterized the expression of kcnq2, kcnq3, and kcnq5 in whole larval zebrafish (Danio rerio) [7], but we know little about the expression of the complement of kcnq genes and the K+ ion channels that they encode in various organs of the adult zebrafish

Summary

Introduction

KCNQx genes encode slowly activating-inactivating K+ channels, are linked to physiological signal transduction pathways, and mutations in them underlie diseases such as long QT syndrome (KCNQ1), epilepsy in adults (KCNQ2/3), benign familial neonatal convulsions in children (KCNQ3), and hearing loss or tinnitus in humans (KCNQ4, but not KCNQ5). Identification of kcnqx potassium channel transcripts in zebrafish (Danio rerio) remains to be fully characterized some genes have been mapped to the genome. A recent study characterized the expression of kcnq, kcnq, and kcnq in whole larval zebrafish (Danio rerio) [7], but we know little about the expression of the complement of kcnq genes and the K+ ion channels that they encode in various organs of the adult zebrafish. The zebrafish offers a unique opportunity to study Kcnq channel modulation, function and dysfunction

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Results

Discussion

Conclusion