The role of rho in bacteriophage T4 development. I. Control of growth and polarity

We have used ts lethal mutants in Escherichia coli termination factor rho to examine its role in T4 development. The rho ts mutation has been transduced into E. coli B from E. coli K12. This mutation has a number of different properties in the E. coli B genetic background, but the overall effect on T4 regulation seems to be the same. Rho-defective bacteria produce T4 after infection but the burst size is lower than in rho + host cells. We have found that two protein bands appear after T4 + infections of rho ts , but not rho + , bacteria. One of these is gp alt and the other is gp 7. These proteins seem to be expressed in a different mode than the late mode in rho + cells. Their appearance is sensitive to a mutation in the T4 mot gene. When T4 + infects E. coli rho + bacteria in the presence of chloramphenicol (CAM), only a subfraction of early RNA is found. This RNA comes from promoter proximal portions of early polycistronic transcription units and is called immediate early RNA (IE). CAM-sensitive RNA is defined as delayed early (DE) RNA. CAM RNA from rho ts bacteria has almost normal amounts of DE RNA. Thus, CAM-induced polarity, which limits T4 transcription to IE RNA, is mediated by rho factor.