An RNA polymerase mutant of Escherichia coli defective in the T4 viral transcription program

Abstract

Some rifampicin-resistant mutants of E. coli, which grow normally, poorly support the growth of bacteriophage T4. One such mutant, Rif R-2, has been studied in some detail. The resistance to rifampicin and the effect on T4 development are cotransduced with arg H and the RNA polymerase is rifampicin resistant, which proves that both effects are due to a mutation in RNA polymerase. The phenotype of T4 development in Rif R-2 has been examined. There is a slight delay in the onset of T4 DNA replication, and at most a slight delay in the synthesis of T4 late messenger RNA, but a considerable delay in the synthesis or assembly of T4 tail fibers. This latter defect is probably sufficient to account for the delay in phage production and can be explained either by a relative inability to make the structural gene products of the tail fibers or through a defect in the synthesis of the gene 57 product—a delayed early T4 protein. Infection of Rif R-2 by T4 results in an incomplete cessation of E. coli specific transcription which may be related to the inability to make tail fibers.