A mutation introduces a premature stop codon into the middle of an exon of a human gene, more than 50 nucleotides upstream of the final exon-exon junction. After splicing, the transcript is rapidly degraded rather than translated. The surveillance pathway responsible is triggered by:
- A Absence of the m7G cap on the mutant transcript
- B Retention of downstream exon junction complexes when a terminating ribosome stalls at the premature stop codon ✓
- C Failure of the poly(A) tail to be added due to loss of the AAUAAA signal
- D Binding of eRF1 instead of a near-cognate aminoacyl-tRNA
Correct answer: B. Retention of downstream exon junction complexes when a terminating ribosome stalls at the premature stop codon
Explanation
Nonsense-mediated decay depends on exon junction complexes deposited 20 to 24 nucleotides upstream of each splice junction. During pioneer translation, if a ribosome terminates more than about 50 nucleotides upstream of the final junction, downstream EJCs remain and recruit UPF proteins, triggering decay. Cap and poly(A) status are unchanged by the mutation, and eRF1 binding occurs in every termination event including normal ones.
Reference: Molecular Biology of the Cell, 7th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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