Nucleotide excision repair (NER) is defective in xeroderma pigmentosum (XP). NER specifically recognises and removes which type of DNA lesion?

• A Bulky helix-distorting adducts including UV-induced cyclobutane pyrimidine dimers and chemical adducts ✓
• B Depurinated abasic (AP) sites from spontaneous base loss
• C Single-base mismatches from replication errors
• D Double-strand breaks from ionising radiation

Explanation

NER specialises in recognising and removing bulky helix-distorting lesions: UV-induced cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts, as well as large chemical adducts (e.g., benzo[a]pyrene-guanine adducts from cigarette smoke). The XPC-RAD23B complex (global genome NER) or stalled RNA polymerase II (transcription-coupled NER) recognises the distortion. Excision involves dual incisions 5' and 3' of the lesion removing a 25–30 nucleotide oligonucleotide. AP sites are repaired by base excision repair (BER). Mismatches are corrected by mismatch repair (MMR, defective in HNPCC/Lynch syndrome). DSBs are repaired by NHEJ or HR.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.