C elegans is an ideal model for genetic studies, Aballay said, because the worm takes only three days to develop from an embryo to an adult capable of reproducing. Also, scientists can easily manipulate specific genes in the worm, and as opposed to other animal models, large quantities of the animals can be grown quickly. They can even be frozen and used at a later date, Aballay said.
Additionally, the worm is essentially a long intestinal tract, which is also advantageous as a model for Salmonella virulence, since a primary target of Salmonella infections in mammals is the intestine. Aballay said this may be the reason of the remarkable overlap between Salmonella virulence factors required for pathogenesis in mammals and worms.
For their experiments, the team used the C. elegans-Salmonella enterica model developed by Aballay. Specifically, the researchers examined one of the bacteria's five known "pathogenecity islands," or clusters of genes that have accumulated in S. enterica bacteria through time. These genes have been acquired by the bacteria through the course of evolution as a way of adapting and improving its chances of successfully infecting its hosts, Aballay explained.
"In this study we have related several genes located in pathogenicity islands to S. enterica pathogenesis in worms," Aballay said.
Within the pathogencity island 1 is the "molecular syringe," known as the Type III secretion system (TTSS). This TTSS punctures the cell wall of the host and injects the virulence factors inside. One of the specific virulence factors injected into the host cells through the TTSS, termed SptP, was critical for the Salmonella's ability to kill C. elegans.
"While there are at least 13 effector proteins, or virulence factors, which are injected into the host through the TTSS, our studies have shown that a single protein (SptP) can have a majo
Contact: Richard Merritt
Duke University Medical Center