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DNA damage prevents the normal enzymatic synthesis of DNA by the replication fork. At damaged sites in the genome, both prokaryotic and eukaryotic cells utilize a number of postreplication repair (PRR) mechanisms to complete DNA replication. Chemically modified bases can be bypassed by either error-prone or error-free translesion DNA polymerases, or through genetic exchange with the sister chromatid. The replication of DNA with a broken sugar-phosphate backbone is most likely facilitated by the homologous recombination (HR) proteins that confer resistance to ionizing radiation (IR). The activity of PRR enzymes is regulated by the SOS response in bacteria and may be controlled by the postreplication checkpoint response in eukaryotes.
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