SOS induction by thermosensitive replication mutants of miniF plasmid.

MiniF, a 9.3 kb fragment of the dispensable F plasmid, carries genes necessary for its replication and partition as well as for the expression of an SOS signal. The arrest of replication of a thermo-sensitive miniFts at 42 degrees C induced SOS functions such as prophage lambda, sfiA expression, W-reactivation of UV-irradiated phage lambda. Two miniF ts9 and ts17 mutations were located within the KpnI fragment (43.6-46.9) in the minimal oriS replicon. Blocking miniF replication by incBC+ incompatibility genes situated in trans on a second plasmid also induced SOS functions. In contrast, if miniFts17 plasmid escaped the replication block at 42 degrees C by being inserted into pR325, there was no SOS induction. SOS induction by the arrest of miniF replication required the miniF lynA+ locus in cis, the host recA+ and lexA+ genes. We found that SOS induction was increased greatly near the stationary phase and that cell viability declined. During host cell exponential growth, miniFts9 and miniFts17 plasmids were lost rapidly, although SOS induction persisted for several cell generations. We postulate that lynA expresses a persistent product that may lead to the unwinding of chromosomal DNA.