摘要：Abstract In E. coli, NusG is an essential regulator of RNA polymerase. Due to its two domain structure, NusG acts as flexible linker in the anti termination complex which promotes elongation rates by suppressing transcriptional pausing in vitro. However the specific role of NusG in the process of N antitermination is still unclear as anti-termination has been observed in the absence of NusG, in vivo. Here we attempt to resolve this issue by isolating a point mutation in NusG that blocks N antitermination. Doing so will reveal the structural interaction between the Nus G and N protein during phage Lambda infection.
