RECOMBINATION-DEFICIENT DELETIONS IN BACTERIOPHAGE AND THEIR INTERACTION WITH CHI MUTATIONS

David Henderson ¹ and Jon Weil ¹

¹ Department of Molecular Biology, Vanderbilt University, Nashville, Tennessee 37235

We have isolated a new class of deletion mutants of phage lambda that extend from the prophage attachment site, att, into the gam and cIII genes. In this respect they are similar to certain of the pbio transducing phage, but they differ in having a low burst size and in forming minute plaques. Lytically grown stocks of the deletions contain a variable proportion of phage that produce large plaques. These have been shown to carry an additional point mutation. Similar mutations, called chi, have been described by Lam et al. (1974), who showed that they result in a hot-spot for recombination produced by the host recombination system (Rec). We show that chi mutations can occur at several sites in the lambda genome and produce a Rec-dependent increase in the burst size of the one deletion tested.—In addition to reducing burst size, the one deletion tested reduces synthesis of DNA and endolysin but increases production of serum blocking protein. A chi mutation partially restores DNA synthesis and endolysin production and reduces serum blocking protein to normal levels. Our results are consistent with the hypothesis put forward by Lam et al., that chi enhances the frequency of Rec-promoted recombination, which provides the only pathway for production of maturable DNA in a red^- gam^- infection. The mechanism of the differential effect on protein production is, however, unclear.—Chi mutations are found to occur in DNA other than that of . We show that, as has been suggested elsewhere (McMilin, Stahl and Stahl 1974), the pbio transducing phages carry a chi mutation within the E. coli DNA substitution. A chi mutation also arose in a new substitution of unknown origin isolated in the course of this work.

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