Genetic code disruptions – outcomes of a nonsense mutation A nonsense mutation in a coding region most typically results in which consequence for the polypeptide product?

Introduction / Context:
Mutations that alter coding sequences can change protein sequence or length. Among these, nonsense mutations convert a sense codon into a stop codon (UAA, UAG, UGA), with major consequences for protein synthesis and function.

Given Data / Assumptions:

• Nonsense mutation introduces an early termination signal.
• Translation machinery halts at premature stop codon.
• mRNA quality-control mechanisms (e.g., nonsense-mediated decay) may decrease mRNA levels.

Concept / Approach:
When a nonsense mutation arises, ribosomes terminate translation prematurely, yielding a truncated protein often unstable or nonfunctional. This is distinct from missense mutations (single amino acid substitutions) and frameshifts (reading-frame disruptions that change length and sequence downstream).

Step-by-Step Solution:
Define nonsense mutation: codon → stop codon.Infer outcome: early translation termination.Predict product: shortened (truncated) polypeptide.Select the option describing premature termination.

Verification / Alternative check:
Clinical genetics frequently links nonsense variants to loss-of-function phenotypes due to truncated proteins or reduced mRNA via surveillance pathways.

Why Other Options Are Wrong:

• Abnormal elongation: would require readthrough or frame changes, not nonsense per se.
• Large in-frame deletion: a structural DNA change, not a single base substitution causing stop.
• mRNA modification: not the typical effect of a nonsense mutation.
• Single amino acid substitution: describes missense, not nonsense.

Common Pitfalls:
Confusing nonsense with missense; assuming all premature stops always yield stable truncated proteins (many are degraded).

Final Answer:
A premature termination of the synthesis of a polypeptide.