Split LexA

LexA is destroyed, gene is activated

SOS system


FIGURE 14.24 RecA and LexA Control the SOS System

Binding of RecA to single-stranded DNA activates RecA so that it cleaves LexA protein. Cleaved LexA protein can no longer bind to DNA and is released. The genes of the SOS system are no longer blocked from transcription. The SOS gene products combat DNA damage.

SOS system

Repair in Eukaryotes 391

FIGURE 14.25 DNA Polymerase V is Part of the SOS System

Activated RecA cleaves LexA dimers, allowing expression of UmuC and UmuD. Two UmuD combine with one UmuC protein and this complex slows replication. DNA repair mechanisms then have time to repair some damage. If the damage is extensive, activated RecA (bound to single-stranded DNA) cleaves UmuD to form UmuD'. When two UmuD' and one UmuC proteins combine, PolV is formed and replicates past any unrepaired damage.

dimer of UmuD' combines with one UmuC, the error-prone PolV (UmuD'2C) is formed (Fig. 14.25).

Like E. coli, yeast, flies and humans all have error-prone DNA polymerases that respond to DNA damage and can replicate past damaged regions. In higher organisms these repair enzymes appear to be more specialized and less error-prone. For example, when human Polymerase Eta passes a symmetrical thymine dimer it usually puts in AA. However, although more accurate, it cannot pass other types of pyrimidine dimers like E. coli PolV. Although this results in a mutation, it is better than complete failure to replicate the DNA.

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