Speciation among the T-even bacteriophages.

Abstract

A system of amber mutants has been developed for each of the T-even phages T2, T6, and RB69. In T2 these mutants identify 53 genes, of which 46 are homologous with T4 genes. The order of genes in the T2 map is virtually identical to that of T4, and recombination in T2 strongly resembles that in T4. In T6 the mutants identify 42 genes, of which 34 are homologous to T4 genes and 3 are homologous to T2 genes not yet identified in T4. The few T6 gene orders which have been determined are the same as in T2 and T4, and T6 recombination resembles that of T2 and T4. RB69 is judged to be a member of the T-even phage species by its serological properties, its particle morphology, and various physical parameters of the RB69 particle and its contained DNA. RB69 mutants identify 37 genes, and their phenotypes are the same as those of T4 mutants. Recombination in RB69 strongly resembles that in T2 and T4, and the distribution of mutant phenotypes around the RB69 map is very much like that of T4. T2, T4, and T6 differ most noticeably in the tail fiber region. Genes 37 and 38 are a unique example of a pair of coadapted genes; T2-T6 combinations of the products of these genes are compatible, whereas T2-T4 and T4-T6 combinations are not. The host range differences between the phages are determined by gene 38. Genes 34 and 35 are genetically much smaller in T2 and T6 than in T4, but there is considerable homology between T2 gene 34 and T4 gene 34. The degree of homology between T2 and T4 decreases from gene 34 to gene 38. In T2-T4 mixed infections T4 excludes T2 by acting against localized exclusion sensitivity determinants near early genes in the T2 genome. This action prevents the T2 genome from participating in the formation of the replicating structure, and it prevents the determinants from appearing among the progeny, but it does not prevent T2 genes from functioning. Markers from the T2 genome appear among the progeny by recombination away from these determinants. The specificity of the T4 action is not controlled by any known T4 gene, nor does it depend on differences between T2 and T4 in DNA glucosylation. The T4-T6 mixed infection is characterized by a depressor effect, and T4 excludes T6 strongly. T6 excludes T2 weakly, and RB69 excludes T2, T4, and T6 very strongly. T4 excludes thirty other newly-isolated T-even phages fairly strongly. A general model has been developed to account for all of these cases of exclusion, and it also accounts for cases of partial exclusion in the T5 and T3-T7 phage species. From the relationships among the T-even phages and their interactions in mixed infections, an attempt is made to reconstruct the evolution of exclusion as a bacteriophage isolating mechanism. Analogies between exclusion and host-controlled modification as a bacterial isolating mechanism are discussed.