Indirect SOS induction is promoted by ultraviolet light-damaged miniF and requires the miniF lynA locus.
Indirect prophage induction is produced by transfer to recipients of u.v.-damaged F plasmid (95 kb). We tested whether the SOS signal can be produced by miniF, a 9.3 kb restriction fragment, coding for the replication and segregation functions of plasmid F. We used lambda miniF, a hybrid phage-plasmid. u.v.-irradiated lambda miniF induced prophages phi 80 or lambda and sfiA, a chromosomal SOS gene, in more than 50% of the infected cells. The maximal inducing dose produced about 0.5 pyrimidine dimers per kb and left 1% of lambda miniF survivors. Thus, the SOS signal produced by u.v.-damaged lambda miniF was almost as potent as that resulting from direct u.v.-irradiation of the lysogens. The u.v.-damaged vector lambda, devoid of miniF, failed to promote SOS induction. In contrast, efficient induction was observed when u.v.-damaged lambda miniF infected a lambda immune host, in which replication and expression of the phage genome were repressed. When replication and expression of the miniF genome was repressed by Hfr incompatibility, SOS induction was largely prevented. All these facts indicate that, in the hybrid lambda-miniF, it is the u.v.-damaged miniF that generates an SOS signal. To locate on the miniF genome the loci that are involved in the production of the SOS signal, we isolated deletions spanning all the miniF restriction fragments. We characterized six mutant phenotypes (Par+, Rep-, Fid-, Par-2, Par-1 and SOS-) related to four functions; partition, copy number, replication and SOS induction. A locus, we call lynA, 800 bp long, located by deletion mapping between the two origins of replication oriP and oriS is required for the production of an inducing signal. We postulate that indirect SOS induction by u.v.-damaged miniF results from the disturbance of the lynA function that may be involved in the co-segregation of F plasmid with the host chromosome.