When T4 infects Escherichia coli in the absence of protein synthesis, rho-mediated termination takes place on early polycistronic transcription units. During the early period of development, the appearance of delayed early transcripts becomes insensitive to the inhibition of protein synthesis. In the absence of the T4 gene product mot, an inducer for the middle mode of transcription, only the early polycistronic messengers are synthesized. In mot- -infected cells, the synthesis of the distal transcripts still becomes completely insensitive to the polar effect of chloramphenicol. This happens because potential rho-sensitive termination sites are not used in these cells. In this respect, overcoming polarity induced by chloramphenicol can be called a process of antitermination. The mot-independent antitermination can be studied by addition of chloramphenicol during infections with mot- bacteriophage. The effect is stable; it allows a constant percentage of rho-sensitive termination sites in the cell to be traversed by RNA polymerase for at least 10 min at 42 degrees C. By examining six different transcription units on the T4 genome, we find that each transcription unit has a cis-acting component (or components) which determines when its rho-sensitive termination site stops functioning. In extreme cases, rho acts with 100% efficiency in some transcription units, whereas it is almost inactive in others.
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