DNA repair 2
DNA Repair Mechanisms
Introduction to DNA Repair
DNA repair involves correcting sequence issues and ensuring the integrity of the genetic material.
Scanning mechanisms are essential as damage locations cannot be predicted.
Two primary types of issues:
Non-standard nucleotides: Incorrect or exotic bases that should not be present.
Mismatch pairs: Normal bases that are paired incorrectly (e.g., G with T).
Repair Strategies
Specialized repair proteins are responsible for correcting errors:
Direct reversal: Straightforward repair of minor modifications.
Excision repair: More involved, involves removing segments of DNA and re-synthesis.
Time-sensitive: Repairs must occur before DNA replication to prevent mutations.
Importance of Tumor Suppressors
P53: A crucial protein acting as a guardian of the genome.
Detects damaged DNA and arrests the cell cycle to allow for repair.
Activates DNA repair proteins in response to damage.
Triggers apoptosis or senescence if damage is irreparable, preventing tumor formation.
Mutations in p53 are frequent in cancers, leading to defective repair systems and increased mutation rates.
Types of DNA Repair Mechanisms
Direct Reversal: Restores normal nucleotides with minimal alteration.
Example: Removal of alkylation modifications (demethylation).
Methyl transferase enzyme restores guanine by transferring unwanted methyl groups.
Special enzymes (e.g., DNA photolyase) can repair cross-links induced by UV light.
Base Excision Repair:
Targets specific damaged bases without affecting the entire nucleotide.
Glycosylases recognize and remove faulty bases, creating abasic sites.
AP endonuclease cleaves the DNA backbone, allowing for restoration via DNA polymerase.
Discrimination between correct bases (T) and incorrect bases (U) ensures proper repair.
Nucleotide Excision Repair (NER):
Removes distorted sections of DNA due to bulky adducts (e.g., benzopyrene).
A protein complex (UvrABC) scans the DNA, binds to distortions, and removes a segment for repair.
Involves specialized helicase to eject the damaged fragment and prepare for replication.
Mismatched Repair:
Identifies and corrects incorrect base pairs (e.g., A pairing with G incorrectly).
Utilizes enzymes like MutS and MutL to distinguish between newly synthesized and template strands.
The MutH protein cleaves the daughter strand for correction, often removing significant DNA segments.
Translesion Synthesis
Specialized polymerases (e.g., pol IV, pol V) can bypass DNA lesions.
They allow for incomplete replication where matching bases might not occur, leading to potential mutations but ensuring DNA synthesis is completed.
Implications of Defective Repair Systems
Disease conditions arising from repair deficiencies include:
Xeroderma Pigmentosum: Genetic defect leads to severe UV sensitivity and skin cancer due to NER failure.
Colon Cancer: Mutations in mismatch repair genes (MutS, MutL) lead to increased mutation rates and cancer risk.
Lung Cancer: Significant damage observed from smoking overwhelms repair mechanisms, resulting in extensive mutations.
Conclusion
DNA repair systems are crucial for genome stability; their impairment can lead to severe health consequences.
Despite repair mechanisms reducing mutation rates significantly, environmental factors like tobacco can vastly increase mutation occurrences, leading to severe diseases such as cancer.