Question

How does the SOS system simultaneously fix damage DNA and increase the mutation rate? How does the SOS system increase the survival of microorganisms?

Answer 1

The SOS response is a coordinated cellular response in E. coli and aids in the survival of the organism by affecting the expression of proteins that are involved in cell division, replication, recombination, and excision repair. The SOS response genes are induced when the bacterial chromosome is extensively damaged; many are involved in DNA repair and mutagenesis. The basic mechanism of regulation is relatively simple. The key regulatory elements are a repressor, called the LexA repressor, and the RecA protein. In E. coli, any block to DNA replication caused by DNA damage produces a signal that activates the E. coli RecA protein. Activation of RecA protein causes autocatalytic proteolytic cleavage of the LexA repressor. Cleavage occurs at a specific Ala-Gly peptide bond. RecA can stimulate protease activity and can promote base pairing between a single strand of DNA and its complement in dsDNA. The LexA repressor regulates the transcription of all the SOS genes. LexA represses SOS response genes by binding to a 20 bp stretch of DNA called an SOS box.

When the DNA is subjected to heavy damage through exposure to UV light or a DNA damaging reagent, DNA repair becomes significantly less accurate and a high mutation rate is observed. DNA replication comes to halt since DNA polymerase III cannot proceed past many types of DNA lesions. RecA also tiggers cleavage of other cellular targets such as UmuD protein. This cleavage activates UmuD and error prone repair system. The current model of the repair system is that the UmuD2UmuC complex binds to a RecA filament near the site of damage, RecA activates the complex by cleaving UmuD to generate UmuD’, and the complex (UmuD’2C or DNA polymerase V) then synthesizes a stretch of DNA to replace the damaged material.

Since proper base pairing is often impossible at the site of a lesion, this translesion replication is error-prone. DNA polymerase V, a Y-family DNA polymerase, lack 3’ à 5’ proofreading exonuclease activity is also known as error-prone DNA polymerase.