Replication of damaged DNA and the molecular mechanism of ultraviolet light mutagenesis.
Crit Rev Biochem Mol Biol
; 28(6): 465-513, 1993.
Article
in En
| MEDLINE
| ID: mdl-8299359
ABSTRACT
On UV irradiation of Escherichia coli cells, DNA replication is transiently arrested to allow removal of DNA damage by DNA repair mechanisms. This is followed by a resumption of DNA replication, a major recovery function whose mechanism is poorly understood. During the post-UV irradiation period the SOS stress response is induced, giving rise to a multiplicity of phenomena, including UV mutagenesis. The prevailing model is that UV mutagenesis occurs by the filling in of single-stranded DNA gaps present opposite UV lesions in the irradiated chromosome. These gaps can be formed by the activity of DNA replication or repair on the damaged DNA. The gap filling involves polymerization through UV lesions (also termed bypass synthesis or error-prone repair) by DNA polymerase III. The primary source of mutations is the incorporation of incorrect nucleotides opposite lesions. UV mutagenesis is a genetically regulated process, and it requires the SOS-inducible proteins RecA, UmuD, and UmuC. It may represent a minor repair pathway or a genetic program to accelerate evolution of cells under environmental stress conditions.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Ultraviolet Rays
/
DNA Damage
/
DNA, Bacterial
/
Mutagenesis
/
DNA Replication
/
Escherichia coli
Language:
En
Journal:
Crit Rev Biochem Mol Biol
Journal subject:
BIOLOGIA MOLECULAR
/
BIOQUIMICA
Year:
1993
Document type:
Article
Affiliation country:
Israel