Fig. 2.

The small deletions in rpoC alter RNAP kinetics in vitro. (A) Comparison of open complex longevity at the rrnB P1 promoter in the absence (gray bars) and presence (white bars) of ppGpp/DksA. All open complex half-life measurements were normalized to wild type. The text above the gray bars is the relative decrease in half-life for each mutant compared with wild-type RNAP. The text in parentheses above the white bars is the relative decrease in open complex half-life in response to the presence of ppGpp/DksA for each RNAP. (B) Comparison of in vitro transcription elongation rate. Elongation was assayed by synchronized transcription on a linear T7 A1 promoter template containing a fragment of the rpoB gene. (C) Comparison of his pause half-lives. Pause half-lives were assayed using reconstituted transcription elongation complexes paused at the his pause site. Pause half-lives were measured at least twice, with the individual values within 10% error of each other. The text above each column denotes the fold decrease relative to wild type. Detailed graphs showing measurements of open complex lifetimes and elongation rates can be found in Fig. S3.