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Repair Processes on Deoxyribonucleic Acid
Author(s) -
Berndt J.
Publication year - 1973
Publication title -
angewandte chemie international edition in english
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.831
H-Index - 550
eISSN - 1521-3773
pISSN - 0570-0833
DOI - 10.1002/anie.197302641
Subject(s) - pyrimidine dimer , dna polymerase , dna ligase , dna , xeroderma pigmentosum , nucleotide excision repair , dna clamp , dna repair , thymine , oligonucleotide , chemistry , photolyase , microbiology and biotechnology , dna polymerase ii , biochemistry , biology , polymerase chain reaction , gene , reverse transcriptase
Many cells have the ability to recognize and eliminate damage to their DNA, particularly thymine dimers formed by UV light. The elimination of this damage may be achieved by enzymatic, light‐dependent cleavage of the dimers into the monomers (photoreactivation) or more frequently by dark repair, in which the damaged part is completely removed from the, DNA. In this repair process, the DNA is incised by an endonuclease in the immediate vicinity of the thymine dimers. Oligonucleotides containing the thymine dimer are removed hydrolytically from the DNA by the 5→3′ exonuclease activity of DNA polymerase I (Kornberg enzyme). The resulting gaps are immediately closed by a de novo synthesis with the aid of the same DNA polymerase I, the complementary strand serving as a template (excision repair). The final step is the formation of the phosphodiester bond between the newly synthesized DNA fragment and the old DNA strand by a DNA ligase. Xeroderma pigmentosum patients lack the endonuclease as a result of a genetic defect; they therefore cannot eliminate thymine dimers from their DNA, and are extremely sensitive to sunlight. All information so far suggests that genetic recombination and DNA repair are performed by the same enzyme system.