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Nucleotide excision repair is similar to base excision repair, but is not preceded by the removal of a damaged base and can act on more substantially damaged areas of DNA.
Brief description:
This repair system includes the breaking of a phosphodiester bond on either side of the lesion, on the same strand, leading to the excision of an oligonucleotide. This excision leaves a gap that is filled by repair synthesis, and a ligase seals the breaks.
The role of uvr system in Nucleotide excision repair:
The uvr system of excision repair in E. coli is the best-studied example. It involves the removal of relatively short, usually 12 nucleotides in length.
ABC excinuclease and its role:
- The key enzyme is made up of three subunits, products of the uvrA, uvrB, and uvrC genes, and is called the ABC excinuclease (Excinuclease= excision endonuclease).
- ABC excinuclease binds to the DNA at the site of a lesion.
- First uvrA and uvrB attach to the DNA at the damaged site.
- UvrA recognizes the damage.
- The departure of uvrA allows uvrC to bind, forming uvrBC dimer which cleaves the damaged strand at the eighth phosphodiester bond on the 5′ side of the lesion and at the fourth or fifth phosphodiester bond on the 3′ side.
- UvrD is a helicase (also called helicase II) that helps to unwind the DNA to allow the release of the single strand between the two cuts. The resulting gap is filled in by DNA polymerase I and sealed by ligase.
Results of defective of this repair mechanism:
In humans, Xeroderma pigmentosum and Cockayne syndrome are caused by genetically defective nucleotide excision repair. Xeroderma pigmentosum, a rare inherited disease, is mainly characterized by the inability of skin cells to repair UV-induced DNA lesions (pyrimidine dimer). Individuals suffering from this autosomal recessive condition are extremely sensitive to sunlight.
The schematic representation of Nucleotide excision repair:
Other related notes:
- Base excision repair: https://thebiologyislove.com/base-excision-repair/
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