One particularly common culprit is the nonsense mutation, where a single incorrect DNA letter inserts a premature stop signal. This allowed the edited cell to override premature stop codons and make full-length proteins without disrupting global protein production. These improvements made the tRNAs more stable and better at decoding premature stop signals. To evaluate its therapeutic potential, they tested the method in cell models of Batten disease, Tay-Sachs disease, and Niemann-Pick C1 disease, all caused by premature stop codons. After installing the engineered suppressor tRNA, enzyme activity in the Batten and Tay-Sachs models rose to 17-70% of their normal levels.

Source: The Hindu February 17, 2026 00:03 UTC