SPO1 and Related Bacteriophages

SPOl, SP82, Fe, 2C, SP8, H1, and SP5C constitute a family of large, virulent bacteriophages of Bacillus subtilis whose distinguishing feature is the complete replacement of thymine by hydroxymethyluracil in their DNA. This chapter focuses on SPO1, about which the most is known, but will also discuss data for the other phages that can illuminate areas not studied with SPO1. Gene product 28 substitutes for the host sigma factor, changing the specificity of the RNA polymerase so that it now transcribes the middle genes, which include genes 33 and 34. The products of these genes then modify the RNA polymerase so that it transcribes the late genes. The gene 27 mutant is also deficient in DNA replication, and neither deficiency appears to be an indirect result of the other. Thus, gp27 may play a direct role in both replication and late transcription, although it remains possible that either deficiency is the result of a polar effect on a downstream gene. All major early promoters are located in the terminal redundancy, as determined either by binding RNA polymerase to specific restriction fragments or by the formation of ternary complexes of restriction fragments, RNA polymerase, and nascent RNA. Recombination is essential for transfection by the DNA of hydroxymethyluracil (hmUra) phages. As shown primarily for SP82, transfecting DNA is susceptible to a host nuclease that causes sufficient damage that recombination between several genomes is necessary to form a single intact genome.