14. A gene encoding t-RNA undergoes a mutational event in its anticodon region that enables it to recognize a mutant nonsense codon and permit completion of translation. Such a mutation is known as
(1) silent mutation
(2) neutral mutation
(3) reversion
(4) Non sense suppressor
A gene encoding t-RNA undergoes a mutational event in its anticodon region that enables it to recognize a mutant nonsense codon and permit completion of translation. The correct answer is (4) Nonsense suppressor.
This mutation alters the tRNA anticodon to base-pair with a premature stop codon (UAG, UAA, or UGA), inserting an amino acid instead of terminating translation, thus producing a full-length protein from a mutated mRNA. Nonsense suppressor mutations are intergenic suppressors, distinct from intragenic ones, and maintain low cellular levels to avoid disrupting normal termination signals.
Option Explanations
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Silent mutation: Changes a codon but encodes the same amino acid due to degeneracy, with no effect on protein sequence or function; it does not alter anticodons or suppress stop codons.
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Neutral mutation: Alters the protein sequence but has no significant impact on fitness or function; it fails to address nonsense codon recognition or translation completion.
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Reversion: Restores the original wild-type sequence in the mutated gene, reversing the defect directly; unlike suppressors, it does not involve a second mutation in tRNA to compensate elsewhere.
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Nonsense suppressor: Matches the query exactly—a tRNA anticodon mutation that reads a nonsense (stop) codon as sense, allowing readthrough and functional protein rescue.
Mechanism of Nonsense Suppression
Nonsense mutations create premature termination codons, leading to truncated proteins via early translation halt. The suppressor tRNA competes with release factors, inserting an amino acid (e.g., tyrosine for UAG) at the stop site, partially restoring protein activity despite potential amino acid substitution. Efficiency depends on tRNA concentration and codon context, making it valuable in genetics research and therapies for diseases like cystic fibrosis.
