Spontaneous hydrolytic deamination converts cytosine residues in DNA to uracil at a measurable rate in every cell. If left unrepaired, this lesion would cause a G:C to A:T transition mutation. Which repair pathway removes it?

• A Nucleotide excision repair
• B Mismatch repair by MutS and MutL homologues
• C Base excision repair initiated by uracil-DNA glycosylase ✓
• D Direct reversal by photolyase

Explanation

Uracil arising from cytosine deamination is a single altered base without helix distortion, which is the hallmark substrate for base excision repair. Uracil-DNA glycosylase cleaves the N-glycosidic bond, creating an AP site that AP endonuclease processes before gap filling. Nucleotide excision repair handles bulky, helix-distorting adducts such as pyrimidine dimers, and photolyase acts only on pyrimidine dimers by light-dependent reversal.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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