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.
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Thesis advisor: Claydon, Thomas
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