A child with ataxia-telangiectasia shows extreme sensitivity to ionizing radiation. Which repair pathway handles the lesion produced by this radiation?
- A Nucleotide excision repair
- B Non-homologous end joining ✓
- C Base excision repair
- D Mismatch repair
Correct answer: B. Non-homologous end joining
Explanation
Ionizing radiation produces double-strand breaks in DNA. In mammalian cells these are repaired mainly by non-homologous end joining, which directly ligates broken ends using the Ku70/Ku80 heterodimer and DNA-PKcs, with ATM coordinating the response. Nucleotide excision repair removes bulky adducts such as pyrimidine dimers, base excision repair removes small deaminated or oxidized bases via glycosylases, and mismatch repair corrects replication errors, none of which address double-strand breaks.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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