coli, Salmonella Typhimurium, Mycobacterium tuberculosis etc, but not in eukaryotic cell. It involves more than 40 gene which encodes protein responsible for protection and replication of DNA as well as repair and mutation. Hence SOS repair causes mutation along with repair of DNA. Thus SOS repair reconstruct the chemical structure of DNA but the heredity information is lost. Error in both complementary strand of DNA would be lethal for cell.However, there also exist an error prone and mutation inducing repair called SOS repair.
Uv photo activation repair free#
Photoreactivation, excision repair and post reactive recombination repair are generally error free repair mechanism.The repair of parent strand is done by DNA polymerase I In this repair mechanism, the gap is filled by sequence information from parent strand of sister chromosome by homologous recombination process.
If a DNA strand contain lesions which prevent base pairing by creating gap in the daughter strand during replication.
It is a double strand break (DSB) repair mechanism. coli and DNA polymerase E in Human and finally joined by DNA ligase.ģ. The excised nucleotide is removed and the resulting gap is filed by DNA polymerase-I in E. The multi sub unit enzyme excinucleases (endonuclease and exonuclease activity) hydrolyses two phosphodiester bond one on either side of distortion caused by lesion creating 3’-OH group and 5’-P group. Unlike base excision repair, the enzymes in nucleotide excision repair recognizes the distortion in shape of double stranded DNA structure caused by thymine dimers or intercalating agents. In nucleotide excision repair mechanism, the defective nucleotide are cut out and replaced. After the damaged nucleotide is removed, the gap is repair by DNA polymerase I and ligated by DNA ligase. The AP site is recognized by AP endonucleases which split the phosphodiester bond on DNA strand at AP site and removes the AP sugar. Glycosylase recognizes and remove the damaged bases by hydrolyzing the glycosidic bond and cut out the damaged base creating AP site (a purinic or pyrimidinic site). Mutation causes alkylation and deamination of bases which are recognized by special DNA glycosylase enzyme. In this mechanism modified bases are recognized and cut out. Excision repair system involves nucleotide repair and base excision repair. The repair system remove and replace the altered bases from damaged DNA. Upto 80% of thymine dimers existing in genome can be photoreactivated. In the dark, the enzyme bind with thymine dimer and in presence of visible light the enzyme split the thymine dimers. This is due to activation of photo reactivating enzyme photolyase, which splits thymine dimer. When UV radiated population of bacteria is subsequently exposed to visible light of wave length of 300-450nm, the survival rate increases and frequency of mutation decreases. A repair mechanism known as photo reactivation can repair this mutation. This pyrimidine dimer formation is lethal to the cell unless it is corrected. Thymine dimer is a state in which two adjacent thymine molecules are chemically joined distorting the structure of DNA, so that impeding transcription and replication process. 
Thymine dimer is most common one but cytosine dimer as well as thymine-cytosine may also occurs. Ultra violet radiation (254 nm) causes formation of pyrimidine dimers (cyclobutane ring), when two pyrimidine bases occurs together in single strand of DNA. Ultraviolet light is a physical mutagen and can induce mutation.
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