the concentration of ssDNA returns to normal levels , cleavage of LexA is terminated -LRB- the lexA gene is itself regulated by LexA -RRB-
the concentration of ssDNA returns to normal levels , cleavage of LexA is terminated -LRB- the lexA gene is itself regulated by LexA -RRB-
Among kanamycin-resistant tranductants , the presence of the lexA ( Ind ) mutation was confirmed through β-galactosidase assay after introduction of the pGE108 plasmid ( Table 2 ) which contains a LexA-regulated cea ∷ lacZ fusion ( Salles et al. , 1987 ) .
However , increased amounts of breaks seem to be associated with increased deletion rates , as shown by previous studies ( 18 , 31 ) , and our demonstration that in a lexA ( def ) mutant overexpressing the translesion polymerases , removal of 3 LexA-controlled endo-nucleases ( uvrB , uvrC , and cho ) causes both a reduction in deletion formation ( Fig. 3 ) and DNA breaks ( Fig .
The increase in mutation rates in the lexA ( def ) mutant required the presence of the LexA-controlled UvrB protein and endonucleases UvrC and Cho .
To examine whether lack of all four translesion DNA polymerases affects expression of other LexA-controlled functions , we used real-time PCR to measure uvrB expression in a lexA ( def ) mutant and a lexA ( def ) mutant lacking all four tranlesion DNA polymerases .
This increase in DNA breaks in the lexA ( def ) strain is mediated by two endonucleases , UvrC and Cho , and the LexAcontrolled UvrB protein ( Koskiniemi and Andersson 2009 ) .