DNA Replication & Repair MCAT Practice Question
A 34-year-old woman with xeroderma pigmentosum presents with multiple skin cancers on sun-exposed areas. Her cells have defective nucleotide excision repair (NER), leading to accumulation of unrepaired UV-induced DNA lesions. Research shows that her fibroblasts are able to complete DNA replication despite the presence of these lesions through activation of translesion synthesis (TLS) polymerases. Which of the following best explains why cells preferentially activate error-prone TLS polymerases rather than stalling replication until NER can remove all DNA damage?
Answer choices
- DTLS polymerases restore normal replication speed by removing DNA lesions before continuing synthesis
- ATLS polymerases possess 3' to 5' exonuclease activity that immediately corrects mispairing at damaged sites
- BTLS polymerases directly reverse UV-induced thymine dimers without requiring additional excision repair
- CCompleting DNA replication despite unrepaired lesions prevents replication fork collapse and the formation of deleterious double-strand breaksCorrect answer
- EActivation of TLS polymerases triggers mismatch repair mechanisms that permanently correct all replication errors within 24 hours
- FTLS polymerases have higher fidelity than standard replicative polymerases and therefore produce fewer mutations
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