Repair of transposable phage M u DNA insertions begins only when the E . coli replisome collides with the transpososome

We report a new cellular interaction between the infecting transposable phage M u and the host E scherichia coli replication machinery during repair of M u insertions, which involves filling‐in of short target gaps on either side of the insertion, concomitant with degradation of extraneous long flanking DNA ( FD ) linked to M u. Using the FD as a marker to follow repair, we find that after transposition into the chromosome, the unrepaired M u is indefinitely stable until the replication fork arrives at the insertion site, whereupon the FD is rapidly degraded. When the fork runs into a M u target gap, a double strand end ( DSE ) will result; we demonstrate fork‐dependent DSEs proximal to M u. These findings suggest that P ol III stalled at the transpososome is exploited for co‐ordinated repair of both target gaps flanking M u without replicating the intervening 37 kb of M u, disassembling the stable transpososome in the process. This work is relevant to all transposable elements, including retroviral elements like HIV ‐1, which share with M u the common problem of repair of their flanking target gaps.