Transcription & Translation MCAT Practice Question
A 3-year-old boy presents with developmental delay, failure to thrive, and progressive neurological deterioration. Genetic sequencing identifies a homozygous missense mutation in the RRF1 gene encoding release factor 1 (RF1), resulting in reduced binding affinity for UAA and UAG stop codons. The child's fibroblasts demonstrate abnormally long polypeptide chains on polyacrylamide gel electrophoresis. Which of the following best explains the molecular basis for this patient's protein abnormalities?
Answer choices
- AImpaired aminoacyl-tRNA synthetase function prevents proper codon-anticodon pairing during elongation
- BIncreased ribosomal frameshifting causes insertion of codons from an alternative reading frame
- CReduced affinity of RF1 for stop codons allows continued addition of amino acids beyond the normal termination pointCorrect answer
- DPremature release of the nascent polypeptide chain at UAA/UAG codons results in truncated protein products
- EEnhanced recruitment of elongation factors EF-Tu and EF-G accelerates translation velocity and disrupts normal termination
- FMutations in the RF1 gene prevent ribosome assembly, leading to decreased overall translation efficiency
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