The global health challenge posed by antibiotic resistant infections is now becoming widely recognized, although there is little agreement on the best strategy to combat this problem. Remarkably, despite the importance of antibiotics, the mechanisms by which they actually inhibit bacterial growth are in many cases unclear. We have recently shown that for one class of antibiotics, which target bacterial protein production, a beautifully simple theoretical model can explain experimental observations that some antibiotics work well for fast-growing cells whereas others are better for slow-growing cells.
This is important because it provides a strategy for targeting acute versus chronic infections. In this project, we will investigate whether similar principles also hold for other types of antibiotics, such as those that target the cell wall or the synthesis of DNA or RNA. This project could be done from a theoretical point of view (constructing and solving simple models) or from an experimental point of view (growing bacteria and measuring their susceptibility to antibiotics), or in a combined approach. Prior biological knowledge is not required.
- Professor Rosalind Allen (School of Physics & Astronomy, University of Edinburgh)
The project supervisor welcomes informal enquiries about this project.
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