Logo image
Transfer RNA mediated restoration of potassium conductance and electrical correction in premature termination Long-QT Syndrome hERG mutants
Journal article   Open access   Peer reviewed

Transfer RNA mediated restoration of potassium conductance and electrical correction in premature termination Long-QT Syndrome hERG mutants

Viggo G. Blomquist, Jacqueline Niu, Papiya Choudhury, Ahmad Al Saneh, Henry M. Colecraft and Christopher A. Ahern
Molecular therapy. Nucleic acids, Vol.34, 102032
12/12/2023
DOI: 10.1016/j.omtn.2023.102032
PMCID: PMC10568093
PMID: 37842167
url
https://doi.org/10.1016/j.omtn.2023.102032View
Published (Version of record) Open Access

Abstract

Disease-causing Premature Termination Codons (PTCs) individually disrupt the functional expression of hundreds of genes and represent a pernicious clinical challenge. In the heart, loss of function mutations in the hERG potassium channel account for approximately 30% of Long-QT Syndrome arrhythmia, a lethal cardiac disorder with limited treatment options. Premature termination of ribosomal translation produces a truncated and, for potassium channels, a potentially dominant negative protein which impairs the functional assembly of the wild-type homotetrameric hERG channel complex. We used high-throughput flow cytometry and patch-clamp electrophysiology to assess the trafficking and voltage-dependent activity of hERG channels carrying patient PTC variants that have been corrected by anticodon engineered tRNA. Adenoviral-mediated expression of mutant hERG channels in cultured adult guinea pig cardiomyocytes prolonged action potential durations and this deleterious effect was corrected upon adenoviral delivery of a human ArgUGA tRNA to restore full-length hERG protein. The results demonstrate mutation specific, context agnostic PTC correction and elevate the therapeutic potential of this approach for rare genetic diseases caused by stop codons. [Display omitted] Loss of function mutations in the hERG potassium channel account for approximately 30% of Long-QT Syndrome arrhythmia, a lethal cardiac disorder with limited treatment options. Blomquist, Niu and colleagues used anticodon engineered tRNA to correct patient nonsense mutations in hERG channels, elevating this therapeutic strategy for other rare genetic diseases.

Details

Metrics

Logo image