Detecting kcnh gene expression using whole mount in-situ hybridization in zebrafish animal model

Long QT Syndrome type II (LQTS2) occurs due to defects in hKCNH2, which encodes the Kv11.1 (hERG) cardiac potassium channel. Multiple hKCNH2 transcripts (hERG1a, hERG1b and hERG-uso) are expressed in cardiac tissue. Studies demonstrate the functional impact of these different hERG transcripts; however, the extent to which and the mechanism(s) by which alternate transcripts are regulated in response to development, environment, or disease variants remains obscure. I have used a zebrafish model system to start to address these questions. In zebrafish, zkcnh6a is the cardiac orthologue of hKCNH2¬, and defects in zkcnh6a are associated with LQTS. In this thesis, I describe the establishment of an approach to design transcript-specific RNA probes and a whole mount in-situ hybridization (WISH) technique to map zkcnh6a and related gene transcript expression in 3-day post-fertilization zebrafish hearts. These studies will aid the development of the zebrafish model in investigating Kv11.1 channel gene plasticity.