ATHENS, Ohio—Scientists have found new genetic information that shows how harmful bacteria cause the acute diarrheal disease shigellosis, which kills more than a million people worldwide each year.
The research, which could lead to the development of future treatments, was published this month in the journal PLoS ONE. The study was led by Ohio University scientist Erin Murphy and doctoral student William Broach, with contributions from University of Nevada, Las Vegas and University of Texas at Austin researchers.
When the disease-causing bacterium Shigella invades a human host, environmental conditions there, such as changes in temperature or pH, stimulate a genetic expression pathway within the bacterium that allows it to survive and cause disease. Central to this genetic pathway are two proteins, VirF and VirB. VirF functions to increase production of VirB which, in turn, promotes the production of factors that increases the bacterium’s virulence, or ability to cause illness in its host.
“It’s like a domino effect," said Murphy, assistant professor of bacteriology in the Ohio University Heritage College of Osteopathic Medicine.
Murphy and Broach’s new study, however, suggests that production of VirB can be controlled independently of VirF. It also shows that the VirF-independent regulation is mediated by a specific small RNA, a special type of molecule whose job is to control the production of particular targets. This is the first study to demonstrate that transcription of virB is regulated by any factor other than VirF, Murphy explained.
