A nonsense mutation introduces a premature stop codon within a coding sequence. What is the most direct molecular consequence typically observed for the gene product?

Introduction / Context:
Point mutations can change a sense codon to a stop codon (UAA, UAG, UGA), producing a nonsense mutation. This event halts translation prematurely and often yields nonfunctional or unstable proteins. Recognizing the consequence helps interpret genetic test results and predict phenotypes.

Given Data / Assumptions:

• The stop codon occurs within the open reading frame before the normal termination site.
• Translation machinery terminates at the premature stop.
• In some eukaryotes, nonsense mediated decay can reduce mRNA abundance, but the primary direct effect is on translation length.

Concept / Approach:
The ribosome releases the nascent polypeptide upon encountering a stop codon, so the produced protein is truncated relative to the wild type. Frameshifts require insertion or deletion not in multiples of three, which is distinct from nonsense. While some transcripts may be targeted for degradation by surveillance pathways, the immediate implication is a shortened protein.

Step-by-Step Solution:
Define nonsense as sense to stop codon conversion. Map ribosome behavior: translation stops at the premature stop. Infer protein outcome: truncated polypeptide. Choose the option describing a shortened protein.

Verification / Alternative check:
Laboratory expression of nonsense alleles yields shorter bands on immunoblot or absent signal due to instability, consistent with truncation.

Why Other Options Are Wrong:

• Premature termination of the mRNA: transcription termination is not the direct effect.
• No effect: contradicts the definition.
• Reading frame shift: caused by indels, not by nonsense substitutions.

Common Pitfalls:
Confusing transcript degradation (a secondary outcome via surveillance) with the primary translation effect of generating a shortened protein.

Final Answer:
shorten the length of the protein encoded by the gene