Perturbation of the SOS Response of Escherichia coli by Plasmids Carrying Truncated recA Genes
Several models for the regulation of E. coli recA+ gene expression and induction of qS functions envisage that the recA+ gene is repressed by the lexA+ gene product. Positive control is thought to occur by “activation” of the basal level of recA+ protein so that it in2ctivates both lexA+ protein and the repressors of the SOS functions2-5. Such models predict that an excess of recA promotor-operato sequences would titrate lexA+ repression of the chromosomal recA+ gene2. The result would be escape synthesis of recA+ protein,and perhaps easier inducibility of SOS functions.To test these naive predictions recA control sequences were introduced into E. coli by transformation with pBR322 derivatives, carr/ing the recA control sequence and 100%, 75% and 20% of the recA+ structural gene (fig.l) pgR1453 and pDR1461 were very generously supplied by Dr. Dean Rupp6.
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