DNA DAMAGE & REPAIR MECHANISMS (SET 2

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What are the most common spontaneous chemical reactions damaging DNA?

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Depurination and deamination are the most frequent spontaneous DNA-damaging reactions.

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How do alkylating agents cause mutations?

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They add alkyl groups to DNA bases, leading to mispairing and mutations if not repaired.

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21 Terms

1
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What are the most common spontaneous chemical reactions damaging DNA?

Depurination and deamination are the most frequent spontaneous DNA-damaging reactions.

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How do alkylating agents cause mutations?

They add alkyl groups to DNA bases, leading to mispairing and mutations if not repaired.

3
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What are reactive oxygen species (ROS), and how do they affect DNA?

ROS are byproducts of metabolism that cause oxidative DNA damage, leading to mutations and genomic instability.

4
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Define DNA adducts.

DNA adduct is a segment of DNA that is covalently bonded to a chemical compound.

These adducts form when mutagenic or carcinogenic chemicals bind directly to DNA, potentially leading to mutations and, over time, cancer if not repaired.

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What are double-strand breaks (DSBs)?

Breaks affecting both strands of DNA; the most severe form of DNA damage, requiring HR or NHEJ for repair.

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What enzyme removes damaged bases in BER?

DNA glycosylase initiates BER by recognizing and excising damaged bases.

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What are the two types of NER pathways?

  1. Global genome NER (GG-NER) – scans entire genome
  2. Transcription-coupled NER (TC-NER) – repairs transcribed strand of active genes
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What types of damage activate p53?

various types of cellular stress and DNA damage, including:

  1. DNA Damage

    • Double-strand breaks (e.g., from radiation)

    • Single-strand breaks or bulky lesions (e.g., from UV light or chemicals)

    • Replication stress

  2. Oncogene Activation

    • Abnormal signals from overactive genes (like Ras or Myc)

  3. Hypoxia

    • Low oxygen levels in the cell

  4. Telomere Shortening

    • Critically short telomeres signal aging or damage

  5. Oxidative Stress

    • Damage from reactive oxygen species (ROS)

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What does p53 do after DNA damage?

Once activated, p53 can:

  • Stop the cell cycle

  • Repair DNA

  • Trigger apoptosis (cell death) if damage is severe

  • Cause senescence (permanent growth arrest)

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What is the role of ATM and ATR kinases in DNA repair?

ATM (Ataxia-Telangiectasia Mutated)

  • Responds toDouble-strand breaks (DSBs)

  • Activates: p53 and CHK2

  • Leads to:

    • Cell cycle arrest

    • DNA repair (homologous recombination)

    • Apoptosis if damage is severe

ATR (ATM and Rad3-related)

  • Responds toSingle-stranded DNA and replication stress

  • Activates: CHK1

  • Leads to:

    • Cell cycle arrest

    • Stabilization of replication forks

    • DNA repair (e.g., nucleotide excision repair)

    • Both activate repair proteins and checkpoints.

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What is the G1/S checkpoint's role in DNA repair?

Ensures DNA is intact before replication begins.

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How do BER and NER interact?

They can collaborate to repair different types of DNA lesions for more efficient repair.

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What are the main repair enzymes?

DNA glycosylases (BER)
Endonucleases (NER, MMR)
DNA polymerases
Ligases
Chromatin remodelers

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What is the function of helicases in DNA repair?

Unwind DNA for NER, HR, and at replication forks; ATP-dependent.

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What happens during replication fork stalling?

Replication halts due to obstacles (lesions, structures, collisions); restart involves protection proteins and translocases.

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What are consequences of replication errors?

Point mutations
Frameshifts
Repeat expansions
Can cause loss of protein function and disease.

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Which DNA polymerase is involved in BER?

DNA polymerase β (Pol β) fills the gap after base removal in BER.

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What is microsatellite instability (MSI)?

Result of defective MMR leading to errors in repetitive DNA sequences.

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What is the role of DNA damage sensors?

Proteins like ATM and ATR detect DNA damage and initiate repair signaling.

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What repair defects are seen in neurodegenerative diseases?

Disrupted BER and NER → genomic instability, neuronal dysfunction (seen in Alzheimer’s, Parkinson’s, Huntington’s)

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What is translesion synthesis prone to?

It's error-prone; specialized polymerases bypass DNA lesions, often introducing mutations.