DNA Replication & Repair MCAT Practice Question
A 34-year-old woman presents with progressive neurodegeneration, recurrent infections, and cancer predisposition. Genetic testing reveals mutations in the APE1 gene, which encodes apurinic/apyrimidinic endonuclease 1. A skin biopsy shows accumulation of unrepaired DNA damage. During base excision repair (BER), uracil DNA glycosylase successfully removes uracil residues from her DNA, creating AP sites. However, without functional APE1, these AP sites persist and accumulate. Which of the following best explains why loss of APE1 function leads to genomic instability in this patient?
Answer choices
- AAPE1 removes the deoxyribose sugar from the AP site backbone, creating a single-strand break that allows subsequent steps of BER to proceedCorrect answer
- BAPE1 synthesizes new DNA nucleotides to fill the gap left by glycosylase action
- CAPE1 ligates the nick in the DNA backbone after polymerase I adds nucleotides
- DAPE1 unwinds the DNA double helix to expose damaged bases for glycosylase removal
- EAPE1 directly removes uracil residues when glycosylase function is impaired
- FAPE1 recruits topoisomerase to relieve DNA tension created during base removal
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