2. A mutation that generates a termination codon is known as:
(a)Missense mutation,
(b)Nonsense mutation,
(c)Reverse mutation,
(d)Silent mutation
What Is a Nonsense Mutation? Understanding Mutations That Generate Termination Codons
Mutations are changes in the DNA sequence that can affect gene expression and protein function in various ways. One critical type of mutation results in the premature termination of protein synthesis. Let’s look at a frequently asked question related to this concept:
Q: A mutation that generates a termination codon is known as:
(a) Missense mutation
(b) Nonsense mutation
(c) Reverse mutation
(d) Silent mutation
Correct Answer:
(b) Nonsense mutation
Explanation:
A nonsense mutation is a type of point mutation in which a single nucleotide change converts a sense codon (that codes for an amino acid) into a stop codon (termination codon). This leads to the premature termination of the translation process, resulting in a truncated and usually non-functional protein.
Here’s how different mutations compare:
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Missense Mutation: Substitutes one amino acid for another; may or may not affect protein function.
-
Silent Mutation: Alters a nucleotide but does not change the amino acid due to codon redundancy.
-
Reverse Mutation: Reverts a mutated sequence back to the original form.
-
Nonsense Mutation: Converts a codon for an amino acid into a stop codon (e.g., UAA, UAG, or UGA).
Example of a Nonsense Mutation:
Original DNA:
5’–ATG AAA GGA TTT–3′
(Met – Lys – Gly – Phe)
Mutation:
5’–ATG AAA TGA TTT–3′
(Met – Lys – STOP)
The codon TGA is a stop codon, so the protein synthesis halts early, losing the downstream amino acids.
Why It Matters:
Nonsense mutations are often associated with genetic disorders and diseases, including certain types of cancer and Duchenne muscular dystrophy, due to the loss of functional protein.
Conclusion:
A nonsense mutation generates a termination codon, ending translation prematurely and resulting in a shortened protein. Understanding this type of mutation is crucial for studies in molecular biology, genetics, and disease research.
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