In the repair of spontaneous depurination and deamination lesions, the enzyme that hydrolyses the N-glycosidic bond to release the abnormal base and create an apurinic or apyrimidinic (AP) site belongs to which pathway?
- A Base excision repair ✓
- B Mismatch repair
- C Nucleotide excision repair
- D Non-homologous end joining
Explanation
Base excision repair begins when a lesion-specific DNA glycosylase, such as uracil-DNA glycosylase acting on deamination-derived uracil, cleaves the N-glycosidic bond and leaves an abasic (AP) site. AP endonuclease then incises the backbone, and short patch repair completes the process. Nucleotide excision repair removes bulky helix-distorting adducts as oligonucleotide fragments rather than single free bases, mismatch repair corrects mispairs, and non-homologous end joining ligates broken ends without glycosylase action.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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