Cell Biology MCAT Practice Question
A 34-year-old woman with a family history of intellectual disability undergoes genetic testing that reveals a heterozygous loss-of-function mutation in PABP1 (poly(A) binding protein 1). Researchers studying her fibroblasts observe abnormal translation termination when analyzing protein synthesis using ribosome profiling. They discover that ribosomes frequently fail to terminate at normal stop codons and instead read through into the 3' untranslated region, producing abnormally elongated proteins. This defect persists even when canonical stop codons (UAA, UAG, UGA) are present in the 3' UTR. Which of the following best explains why PABP1 dysfunction leads to read-through translation despite the presence of functional stop codons?
Answer choices
- APABP1 mediates mRNA circularization through interaction with eIF4G, which enhances the efficiency of termination factor recognition at stop codonsCorrect answer
- BPABP1 directly recruits and phosphorylates eRF1 to increase the catalytic activity of the peptidyl transferase center
- CPABP1 prevents ribosomal frameshifting through stabilization of mRNA secondary structures in the 3' UTR
- EPABP1 competes with eIF3 for ribosome binding, allowing eRF3 to access the A site
- DPABP1 protects the poly(A) tail from deadenylase degradation, which is required to trigger ribosome release at stop codons
- FPABP1 inhibits the translation initiation machinery to prevent ribosome recycling and rebinding to downstream AUG codons
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