The UvrABC Repair Mechanism Repairs DNA Damage Caused by Bulky Chemical Adducts

DNA is constantly exposed to various damaging agents, including chemicals, radiation, and environmental mutagens. Cells have evolved multiple repair mechanisms to maintain genomic integrity. In bacteria like Escherichia coli, the UvrABC endonuclease complex plays a critical role in repairing DNA lesions, especially those caused by bulky chemical adducts that distort the DNA helix.

What Is the UvrABC Repair Mechanism?

The UvrABC repair system is a multienzyme complex involved in nucleotide excision repair (NER) in bacteria. It recognizes and removes a wide variety of DNA lesions that cause significant distortion of the double helix, such as:

• Pyrimidine dimers formed by UV radiation

• Bulky chemical adducts from mutagenic chemicals

• Other helix-distorting DNA damages

The complex is composed of three proteins encoded by the uvrA, uvrB, and uvrC genes:

• UvrA: Functions as the initial damage sensor, detecting distortions in the DNA helix.

• UvrB: Binds to the damaged site and helps verify the lesion.

• UvrC: Performs dual incisions on the damaged DNA strand, cutting on both sides of the lesion.

How Does the UvrABC Complex Work?

1. Damage Detection:
   The UvrA dimer, often in complex with UvrB, scans DNA for structural distortions caused by bulky lesions.

2. Damage Verification:
   Upon detecting damage, UvrA dissociates, and UvrB binds tightly to the lesion, stabilizing the complex.

3. Dual Incision:
   UvrC binds to UvrB and catalyzes two cuts in the damaged strand: one 4–5 nucleotides downstream and another 8 nucleotides upstream of the lesion, excising a 12–13 nucleotide segment containing the damage.

4. Excision and Repair Synthesis:
   DNA helicase II (UvrD) removes the excised oligonucleotide. DNA polymerase I fills the gap by synthesizing new DNA using the undamaged strand as a template, and DNA ligase seals the nick.

What Types of DNA Damage Does UvrABC Repair?

The UvrABC system specializes in repairing bulky lesions that cause helix distortions, including:

• Bulky chemical adducts: Large chemical groups covalently attached to DNA bases, such as those caused by carcinogens and environmental toxins.

• UV-induced pyrimidine dimers: Cyclobutane pyrimidine dimers and 6-4 photoproducts.

• Other helix-distorting lesions: Such as certain crosslinks and oxidative damage.

Why Other Options Are Incorrect

• (1) Missing bases:

  • Missing bases (abasic sites) are typically repaired by base excision repair (BER), not UvrABC.

• (2) Strand breaks:

  • Strand breaks are repaired by pathways such as homologous recombination or non-homologous end joining, not by UvrABC.

• (3) Cross-linked strands:

  • Interstrand crosslinks require more complex repair involving recombination and specialized pathways; UvrABC can initiate repair but is not solely responsible.

Correct Answer

(4) DNA damage caused by “bulky” chemical adducts

Related Keywords for SEO Optimization

• UvrABC repair mechanism

• Nucleotide excision repair (NER)

• Bulky DNA adduct repair

• DNA damage recognition

• Pyrimidine dimers repair

• DNA excision and synthesis

• UvrA, UvrB, UvrC proteins

• DNA helicase II (UvrD)

• DNA polymerase I and ligase in repair

• DNA repair pathways in bacteria

• DNA damage by chemical mutagens

• DNA repair enzymes

• Helix-distorting DNA lesions

Conclusion

The UvrABC repair mechanism in bacteria is primarily involved in repairing DNA damage caused by bulky chemical adducts that distort the DNA double helix. This system recognizes the lesion, excises a short damaged DNA segment, and facilitates repair synthesis and ligation. Therefore, among the given options, the correct answer is:

(4) DNA damage caused by “bulky” chemical adducts.