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DNA repair by : S. Solali

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Types of DNA Damage 1.Deamination: (C U and A hypoxanthine) 2.Depurination: purine base (A or G) lost 3.T-T and T-C dimers: bases become cross- linked, T-T more prominent, caused by UV light (UV-C (

The SOS response In response to extensive genetic damage there is a regulatory system that co-ordinates the bacterial cell response. This results in the increased expression of >30 genes, involved in DNA repair, these include: recA - activator of SOS response, recombination sfiA (sulA) - a cell division inhibitor (repair before replication) umuC, D - an error prone bypass of thymine dimers (loss of fidelity in DNA replication) uvrA,B,C,D - excision repair The SOS response is regulated by two key genes: recA & lexA

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SOS LexA normally represses about 18 genes SOS regulon includes lexA (autoregulation), recA, uvrA, uvrB, uvrC, umuDC, sulA, sulB, and ssb sulA and sulB, activated by SOS system, inhibit cell division in order to increase amount of time cell has to repair damage before replication. Each gene has SOS box in promoter. LexA binds SOS box to repress expression. However, LexA catalyses its own breakdown when RecA is stimulated by ssDNA.

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SOS SOS repair is error-prone. This is why UV is a mutagen. May be due to RecA binding ssDNA in lesions, which could then bind to DNA Pol III complex passing through this area of the DNA and inhibit 3'>5' exonuclease (proofreading) ability. This makes replication faster but also results in more mutations. This affect on proofreading seems to involve UmuD'-UmuC complex as well. RecA facilitates proteolytic cleavage of UmuD to form UmuD'. The UmuD'-UmuC complex may bind to the RecA-Pol III complex and promote error-prone replication.

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SOS Also allows Pol III to replicate past a T-dimer but introduces many mutations while doing so Once damage is repaired, RecA no longer catalyzes cleavage of LexA (which is still being made), so uncleaved LexA accumulates and turns the SOS system off.