The SOS response is induced by replication fork blockage at a Ter site located on a pUC-derived plasmid: dependence on the distance between ori and Ter sites.
A new model system for the study of the SOS response has been developed. In this system the response is induced by blocking the replication fork at a Ter site located in pUC-derived plasmids. Blockage of the fork is dependent on the expression of the Ter binding protein, Tus, encoded on another plasmid, in which the tus gene is under the control of the ara promoter. SOS induction can, therefore, be controlled by arabinose. The extent of the SOS response was monitored by measuring the activity of beta-galactosidase, expressed from a lacZ gene fused to the 5' region of the sfiA gene, a typical SOS-responsive gene. Expression of the fusion gene is completely dependent on recA+ and lexA+ genes. Using this system, we found that the distance between the ori and Ter sites is directly correlated with the strength of SOS induction. The properties of this system are discussed.
Taki
K
K
Department of Molecular Biomechanics, The Graduate University for Advanced Studies and National Institute for Basic Biology, Okazaki, Aichi, Japan.
Horiuchi
T
T
D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D001665:Binding Sites; D004261:DNA Replication; D004269:DNA, Bacterial / Q000096:biosynthesis; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D004926:Escherichia coli / Q000235:genetics*; D029968:Escherichia coli Proteins; D010957:Plasmids; D018741:Replication Origin; D013014:SOS Response, Genetics
D001426:Bacterial Proteins; C062011:DNA replication terminus site-binding protein, E coli; D004269:DNA, Bacterial; D004268:DNA-Binding Proteins; D029968:Escherichia coli Proteins