Ham22, a mini-F mutation which is lethal to host cell and promotes recA-dependent induction of lambdoid prophage.

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Abstract
A mini‐F region 800 bp long, located between the two F origin sites, plays an essential role in the relationship between the F plasmid and its host. This region comprises two sets of overlapping coding sequences: the first set codes for the newly identified H1 and H2 polypeptides; the second set codes for polypeptides G1 and G2. A mini‐F amber mutation (Ham22) causes the virtual disappearance of polypeptides H1 and H2 but only slightly reduces synthesis of polypeptides G1 and G2. This mutation: (i) renders mini‐F hybrids lethal to the host cells (conditional Hos‐ phenotype for host survival) and (ii) causes the induction of a resident prophage in recA+ strains (conditional Map‐ phenotype for maintenance of the prophage). When an additional mutation prevents the synthesis of polypeptides G1 and G2, both the lethal character and the induction of the prophage are abolished. We conclude: (i) that polypeptides G1 and/or G2 are specific mini‐F polypeptides involved in the plasmid‐mediated killing effect and in the recA‐dependent induction of the resident prophage and (ii) that, in normal conditions, polypeptides H1 and/or H2 negatively control (directly or indirectly) the action of polypeptides G1 and/or G2. In relation to the analysis of indirect induction mediated by u.v.‐irradiated lambda mini‐F hybrids, we propose that polypeptides G1 and/or G2 are specific mini‐F products involved in the activation of the bacterial SOS pathway. The H1/H2 and G1/G2 polypeptides could constitute the controlled mini‐F signal enabling the coordination between cell division and F plasmid replication.