The dormancy-specific regulator, SutA, is intrinsically disordered and modulates transcription initiation in Pseudomonas aeruginosa

SutA is upregulated during growth arrest in Pseudomonas aeruginosa and binds RNA polymerase (RNAP), causing widespread changes in gene expression. Using biochemical, structural and genetic methods, we examined how SutA interacts with RNAP and the functional consequences of these interactions. SutA consists of a central α-helix with unstructured N and C-terminal tails. It binds to the β1 domain of RNAP and competes with DNA, leading to effects that are either activating or repressing, depending on the sigma (σ) factor and promoter. Our data suggest that SutA is unlike conventional DNA-binding transcription factors, in that interactions between its α-helix and RNAP allow its acidic N-terminal tail to modulate the path of DNA within the transcription initiation complex, while its C-terminal tail stabilizes its interaction with RNAP. These activities help enhance expression of diverse genes, including essential ones such as the ribosomal RNA operons, under conditions of long term resource limitation.