Fig. 9: ρ regulation under optimal growth and stress conditions.
Top, under optimal growth conditions bulk mRNA synthesis is protected from premature termination by ρ through transcription-translation coupling66,67. A specific transcription anti-termination complex (rrnTAC) shields the ribosomal RNAs from ρ10. Bottom, under stress conditions, when translation is inefficient, ρ activity must be regulated. Phages use different strategies to protect transcription of their own genomes. Similar to the rrnTAC, lambdoid phages rely on specific anti-termination complexes, such as λN-TAC, to shield the nascent transcript from ρ11. Phage P4 uses the Psu protein that directly binds to ρ and thereby prevents the formation of termination complexes38. To date, three cellular proteins are known to directly bind ρ and inhibit termination, but other stress-specific regulators likely exist. YihE is induced upon periplasmatic stress44,53, whereas stress conditions under which Hfq and Rof regulate ρ activity remain to be identified. YihE binds the ρ NTD, inhibiting ρ-RNA interactions20; the mechanism of ρ regulation by Rof has been determined in this study, and molecular details of Hfq-mediated ρ inhibition remain to be solved16,19. By directly binding ρ, each of these anti-terminators may interfere with the formation of ρ-dependent termination complexes that assemble in an EC-dependent manner (center left)33,34 or RNA-dependent manner (center right)24,48.
