The quarternary structure of complex IV of the electron transport chain of Drosophila melanogaster is a key study of Prof. Bill Ballard.
Evolution of Shigella Virulence
Shigella causes over 160 million cases of infection with 1 million deaths worldwide. There is currently no vaccine available and antibiotic resistance has become a serious issue in developing countries. Understanding the evolution of virulence and pathogenesis of Shigella will help us design preventative measures.
The evolution of Shigella as a pathogen is unique among the known human bacterial pathogens in that there exist several distinctive lineages derived from the same species E. coli. In addition, there is also enteroinvasive E. coli which shares the same mode of pathogenesis and may be viewed as an evolutionary intermediate of Shigella, giving us another unique form for comparison to understand the evolution of Shigella virulence. Studies have shown that for Shigella became a pathogen through not only gain of virulence genes but also loss of “antivirulence” genes. Lysine decarboxylation has been shown to be anti-virulence in Shigella as the by-product attenuates virulence by inhibition of iron-regulated enterotoxins. In this project, we will determine the damages in Shigella genomes through genetic analysis, in particular pathways that are damaged in multiple lineages which are likely to be important in virulence. We will determine the effect of selected metabolic pathways on Shigella virulence using C. elegans as an in vivo model. The project involves genome analysis, PCR and sequencing.
Selected references (available upon request)
- Lan, R., and P. R. Reeves. 2002. Eschericheria coli in disguise: molecular origins of Shigella. Microbes and Infection 4:1125-1132.
- Maurelli AT. 2007. Black holes, antivirulence genes, and gene inactivation in the evolution of bacterial pathogens FEMS Microbiology Letters 267:1-8.
BABS personnel that are responsible for this project