Chronic Pseudomonas aeruginosa infections, a major cause of morbidity and mortality for CF patients, are highly resistant to antibiotic treatment, and many lines of evidence suggest that this is due in part to slow-growing states imposed by the lung environment. In previously published work (Babin BM, et al. Proc Natl Acad Sci 2016;113(5):E597-605), we identified a novel RNA polymerase-binding protein that is post-transcriptionally upregulated under such slow-growth conditions. We named this small, acidic protein SutA, and showed using RNA-Seq and ChIP-Seq that it associates with RNA polymerase (RNAP) at many genomic regions, and tends to positively affect transcript levels for genes with which it associates. The genes that are affected include ribosomal RNA and protein genes, and other genes with roles in metabolism and stress survival. Furthermore, we showed that deletion of the sutA gene confers a disadvantage on cells subjected to fluctuations between growth-arrested and growth-promoting states. Thus, SutA may contribute to survival of Pseudomonas aeruginosa in environments like the CF lung, where oxygen and nutrient availability are likely to be heterogeneous in time and space.
Bergkessel, M., Newman, D. K., Babin, B., & Tirrell, D. A. (2017). SutA is a Global Transcriptional Regulator Operating during Slow Growth in Pseudomonas Aeruginosa. Pediatric Pulmonology, 52(S47), S366-S367. . https://doi.org/10.1002/ppul.23840