Mechanisms and Consequences of Post-Transcriptional Gene Regulation in Bacterial Pathogens

The regulatory mechanisms that control bacterial gene expression are diverse and include factors that influence DNA copy number, mRNA transcription and stability, protein translation, modification, and turnover. The ability to integrate these many and varied mechanisms to optimize gene expression is critical for the adaptation of the cell to new environmental niches, changing conditions, and the presence of stressors. This is particularly true for bacterial pathogens, which must also subvert host defenses during infection. The modulation of gene expression via post-transcriptional mechanisms, that is, after mRNA has been synthesized but prior to post-translational regulatory effects, is an essential component of the regulatory architecture of the cell and allows the bacterium to more rapidly respond to its changing environment. These mechanisms include cis- and trans-acting small, non-coding RNAs, RNA-binding proteins, riboswitches, thermosensors, RNases, and Type I toxin-antitoxin systems, and may result in changes in RNA stability, efficiency of ribosome binding, translation initiation, and transcript secondary structures. Recent advances in the field have added to our understanding of how post-transcriptional gene expression influences the virulence of bacterial pathogens, its impact on gene expression programs during infection, and the specific vs. shared regulatory mechanisms that underlie the optimal production of virulence factors during disease. This Research Topic is focused on the latest advances in our understanding of the post-transcriptional processes that contribute to gene regulation in bacterial pathogens and addresses both the mechanisms of said regulation as well as the consequences on the pathogen as well as the host.