“…Such an association raises a question as to what regulates Rho outside ORFs (notably during transcription of long leader regions) when there is no ribosome trailing behind RNAP to increase its processivity (Proshkin et al, 2010) nor to prevent the mRNA from associating with Rho (Roberts et al, 2008;Rabhi et al, 2010). One possibility is that, as observed during transcription of ribosomal rrn operons or bacteriophage l chromosome (reviewed in Condon et al, 1995;Roberts et al, 2008;Sen et al, 2008), accessory factors bind, in a conditional manner, to RNA and/or to the transcription machinery to form an antitermination complex resistant to Rho. Antitermination complexes that resist to Rho-dependent termination signals within rrn and l operons contain the NusA, NusB, NusE (ribosomal protein S10), and NusG factors as well as specific factors such as bacteriophage N protein for lN antitermination or ribosomal proteins (S2, S4, L1, L3, L4, and L13) and other unidentified cellular factor(s) for rrn antitermination (Condon et al, 1995;Torres et al, 2001;Roberts et al, 2008;Sen et al, 2008). Both rrn and lN antitermination complexes are stabilized by elaborate networks of interactions among their many components that include binding of a NusB-NusE heterodimer to a boxA RNA sequence found in the rrn and l transcripts (Roberts et al, 2008;Sen et al, 2008) and binding of NusG to RNAP through its N-terminal domain (NusG-NTD) and to NusE through its C-terminal domain (NusG-CTD; Mooney et al, 2009b;Burmann et al, 2010).…”