Скачать или смотреть 2. DNA Replication & Repair | Enzymes, Mechanisms & Clinical Disorders | MBBS Biochemistry | USMLE

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DNA Replication & Repair | Enzymes, Mechanisms & Clinical Disorders | MBBS Biochemistry | USMLE Step 1

👋 Future doctors! Every time a cell divides, it must faithfully replicate DNA — and when mistakes occur, the cell relies on DNA repair mechanisms. If these fail, mutations accumulate, leading to genetic diseases and cancer.

This lecture simplifies the mechanism of DNA replication, key enzymes, and repair pathways, with integrated clinical correlations. Essential for MBBS, NEET PG, FMGE, and USMLE Step 1 prep. 🧬📚

🌟 DNA Replication
Basic Features:
• Semi-conservative, semi-discontinuous, bidirectional.
• Origin of replication → replication forks → leading & lagging strands.

Key Enzymes:
• Helicase – unwinds DNA.
• SSB proteins – prevent reannealing.
• Topoisomerase – relieves supercoils (targets of fluoroquinolones, etoposide).
• Primase – lays RNA primer.
• DNA Polymerases:
– Prokaryotes: Pol III (elongation), Pol I (primer removal, gap filling).
– Eukaryotes: Pol α (priming), Pol δ (lagging strand), Pol ε (leading strand), Pol γ (mitochondria).
• Ligase – seals nicks between Okazaki fragments.
• Telomerase – maintains telomeres using an RNA template (active in stem cells & cancers).

🌟 DNA Repair Mechanisms

1️⃣ Proofreading by DNA Polymerase – 3’→5’ exonuclease removes mispaired bases.

2️⃣ Mismatch Repair (MMR): fixes replication errors missed by proofreading.
• Defect → Lynch syndrome (HNPCC).

3️⃣ Base Excision Repair (BER): repairs small non-bulky lesions (deamination, depurination).
• Uses glycosylase, AP endonuclease.

4️⃣ Nucleotide Excision Repair (NER): removes bulky adducts like UV-induced thymine dimers.
• Defect → Xeroderma Pigmentosum (XP).

5️⃣ Double-Strand Break Repair:
• Homologous recombination (HR): error-free.
• Non-homologous end joining (NHEJ): error-prone.
• Defects → BRCA1/2 cancers, Ataxia-telangiectasia.

🩺 Clinical Correlations

XP: NER defect → extreme UV sensitivity, skin cancers.

Lynch Syndrome: MMR defect → colorectal cancer.

Ataxia Telangiectasia: defective NHEJ → neurodegeneration, immunodeficiency, radiosensitivity.

Fanconi Anemia & Bloom Syndrome: DNA repair defects → aplastic anemia, malignancy.

Anti-cancer drugs: methotrexate, cisplatin, and topoisomerase inhibitors target replication/repair.

🎯 Exam Integration

G≡C has 3 bonds, A=T has 2 bonds (more GC = more stable DNA).

Okazaki fragments = lagging strand.

NER defect = Xeroderma Pigmentosum.

MMR defect = Lynch Syndrome.
👉 A classic USMLE & NEET PG area for both recall and case-based questions.

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❓Should we make a separate focused video on DNA Repair Disorders (XP, Lynch, AT, BRCA) with case-based vignettes? Drop your request in the comments! 😊

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