Double-strand breaks produced by ionizing radiation in quiescent (G0) mammalian cells are repaired predominantly by which mechanism?
- A Nonhomologous end joining mediated by Ku proteins and DNA-PKcs ✓
- B Homologous recombination using the sister chromatid as template
- C Base excision repair by glycosylases and AP endonuclease
- D Transcription-coupled nucleotide excision repair
Explanation
Nonhomologous end joining operates throughout the cell cycle and is the dominant double-strand break pathway in G0 and G1, where no sister chromatid exists as a template. The Ku70/Ku80 heterodimer binds broken ends and recruits DNA-PKcs, ligase IV, and XRCC4 to religate ends, often with small sequence loss. Homologous recombination predominates in late S and G2. Base excision and nucleotide excision repair handle single-base and bulky lesions respectively.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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