Formation of phage T1 concatemers by the RecE recombination pathway of Escherichia coli.

Infections of nonpermissive ( sup0 ) Escherichia coli by T1 phage with amber mutations in either gene 3.5 or gene 4 exhibit a variety of defective phenotypes, including premature arrest of T1 DNA synthesis, failure to make concatemeric DNA, formation of an abnormal DNA replication intermediate, failure to package phage DNA, and reduced genetic recombination. The lethal effect of gene 3.5 or 4 mutations is suppressed when the sup0 bacteria express the RecE recombination pathway. This RecE suppression occurs by partial restoration of the capacity to make concatemeric molecules and partial reversal of the DNA arrest defect which, in turn, leads to the formation of viable progeny. Infection by T1+ or by mutants defective in any of the four DNA synthesis genes (genes 1, 2, 3.5, and 4) inhibited the ATP-dependent exonuclease present in uninfected cells (presumably the RecBC enzyme, exonuclease V). Extracts from T1+ infections also showed increased levels of an ATP-independent exonuclease activity which was absent from gene 4 mutant extracts. It is concluded that gene 4, together with gene 3.5, specifies an activity related to that of the RecE exonuclease VIII and essential for T1 concatemer formation and recombination.