## DNA Repair Mechanisms in Eukaryotes ### Overview of Major Repair Pathways **Key Point:** Eukaryotes employ multiple DNA repair mechanisms, each specialized for different types of damage. NHEJ is a major DSB repair pathway, but it does NOT require sequence homology. ### Comparison of DNA Repair Pathways | Repair Pathway | Type of Damage | Key Feature | Homology Requirement | |---|---|---|---| | Nucleotide Excision Repair (NER) | Bulky lesions, thymine dimers (UV) | Removes 25–30 nucleotide segment | Not required | | Mismatch Repair (MMR) | Post-replication errors | Recognizes mismatches and corrects | Not required | | Base Excision Repair (BER) | Oxidative damage, alkylation | DNA glycosylase initiates | Not required | | Homologous Recombination (HR) | Double-strand breaks | Uses sister chromatid as template | **Required** | | Non-Homologous End Joining (NHEJ) | Double-strand breaks | Direct ligation of broken ends | **NOT required** | **High-Yield:** NHEJ is a "quick and dirty" DSB repair mechanism that directly ligates broken DNA ends without requiring sequence homology. This makes it error-prone but fast. In contrast, HR requires extensive homology and is more accurate. ### Correct Statements 1. **NER removes thymine dimers** — True. NER is the primary pathway for removing UV-induced thymine dimers and other bulky lesions. 2. **MMR corrects post-replication errors** — True. MMR detects and corrects mismatches that escape proofreading by Pol δ. 3. **BER initiated by DNA glycosylase** — True. BER is the first step in removing damaged bases from the DNA backbone. 4. **NHEJ requires homology** — FALSE. NHEJ is homology-independent and directly ligates DSB ends. **Clinical Pearl:** Defects in NER cause xeroderma pigmentosum (XP), a condition with extreme UV sensitivity and high skin cancer risk. Defects in NHEJ components (e.g., Ku70/80, DNA-PKcs) impair DSB repair and increase cancer risk. **Mnemonic:** "**HR** = **H**omology **R**equired; **NHEJ** = **N**o **H**omology **E**ver **J**oined."
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