DNA Replication & Repair MCAT Practice Question
A patient presents with xeroderma pigmentosum (XP), a rare genetic disorder characterized by extreme UV sensitivity and high skin cancer risk. Genetic analysis reveals a deficiency in nucleotide excision repair (NER) enzymes. When fibroblasts from this patient are exposed to UV light, thymine dimers accumulate and are not removed. Which DNA repair mechanism is primarily defective in this patient, and what is the likely consequence of this deficiency?
Answer choices
- ABase excision repair (BER) is defective, resulting in inability to repair oxidative damage to DNA bases
- BNon-homologous end joining (NHEJ) is defective, resulting in inability to repair double-strand breaks from UV radiation
- CMismatch repair (MMR) is defective, resulting in accumulation of replication errors and point mutations
- DNucleotide excision repair (NER) is defective, resulting in inability to remove bulky DNA adducts and pyrimidine dimersCorrect answer
- EDirect reversal repair is defective, preventing photolyase from repairing thymine dimer cross-links
- FHomologous recombination repair (HR) is defective, resulting in inability to resolve UV-induced DNA interstrand crosslinks
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