Evidence that mutations in the suA polarity suppressing gene directly affect termination factor rho

Abstract

THE suA mutation in Escherichia coli is defined by its suppression of the polar effects of nonsense mutations on distal genes¹. Richardson et al.² discovered that two independent mutations in the suA gene affect the transcriptional termination factor rho. This suggests² a mechanism for polarity: as long as ribosomes progress along the nascent message, transcription proceeds; but when ribosomal progress is blocked, exposure of the distal RNA somehow causes rho to terminate transcription prematurely. As others have noted^3–6, the involvement of rho in translational polarity could explain several puzzling observations concerning the control of both transcription and translation. Richardson et al.² proposed that rho may be the product of the suA gene. They hesitated to draw that conclusion, however, because they found a rather high level of rho activity, 9% of wild type, in a strain believed⁷ to contain an amber mutation in the suA gene (strain 2055). Either this amber lesion was extraordinarily leaky or, alternatively, the absence of suA gene function only partially and indirectly diminished the level of rho activity in the cell. The experiments reported here clarify this problem and argue that the transcriptional termination factor rho is indeed the direct protein product of the suA gene.