Autogenous regulation of transcription termination factor Rho

Abstract

We present evidence that the transcription termination factor Rho is autogenously regulated in Escherichia coli. The steady-state level of Rho is increased approximately tenfold in rho mutant cells. In the rho+ revertants, the content of Rho is similar to the wild-type level. A rho-/rho+ merodiploid produces equimolar amounts of the mutant and the wild-type Rho polypeptides, both at a reduced level compared to the mutant. The steady-state level of rho messenger RNA is also increased in a rho mutant. A rho-galK transcriptional fusion produces at least tenfold more galactokinase in a rho- strain than in a rho+ strain. In vitro, in a coupled transcription-translation system, the synthesis of Rho protein is specifically inhibited by wild-type Rho but not by Rho15 mutant protein. Anti-Rho antibody specifically stimulates Rho synthesis in the rho+ extract but not in a rho- extract. We suggest that the autogenous regulation of Rho involves premature transcription termination within the rho gene. Regulation of Rho level may provide the cell a mechanism to modulate the expression of genes which are separated from their promoters by Rho-dependent termination signals.