The microbiology department held a three day writing seminar for UAB students and postdoctoral employees in May 2019. The purpose of which was to teach graduate students and post‐docs how to effectively communicate science to a lay audience. The department invited Dr. Nicki LeBrasseur, the senior director of scientific communications at DNA Communications to instruct the on and off campus portions of the course. The students were tasked with writing a press release on an assigned paper and were given feedback. Sara Stoner (Scoffield lab) participated in the workshop and her article featuring Dr. Gray's research is below.

Survival Under Stress: New Findings on How Bacteria Adapt to Hostile Conditions

In order to cause infections, bacteria must quickly adapt to hostile conditions created by the human body. For example, our bodies contain immune system cells, competing bacteria, a lack of nutrients, and harmful compounds that bacteria must overcome to thrive and spread infection. Bacteria’s ability to sense changes in their surrounding environment and rapidly respond to those changes is known as the stress response. Research by Dr. Michael Gray at the University of Alabama at Birmingham has recently uncovered new ways in which stress response systems are regulated by bacteria. Understanding what controls stress responses can help us create therapeutics that prevent harmful bacteria from being able to adapt and survive in humans.

Polyphosphate (polyP) is a key molecule in kickstarting the various bacterial stress response systems, but little is known about how bacteria regulate polyP production. This molecule has been conserved in organisms for over a billion years, and many pathogens require its presence to cause disease. For the last 20 years, scientists thought polyP production was controlled by activation of the stringent response, which is a specific stress response of bacteria in reaction to nutrient starvation, heat shock, and other stressful conditions. But Dr. Gray’s research shows that the stringent response is not required for polyP regulation, disproving this long-established hypothesis. Instead, Dr. Gray has discovered that polyP production is regulated by a protein called DksA, which controls expression of a wide variety of genes in E. coli. This important correction to the widely known model of polyP regulation brings us closer to understanding how bacteria use stress response systems to persist and cause infections. Discovering components that are important for controlling stress response molecules such as polyP could potentially lead to the development of therapeutics that target these molecules and therefore prevent harmful bacteria from thwarting the many ways in which we try to kill them.