Dr. R. Fredrik Inglis

About Me

I am currently an ETH Postdoctoral Fellow in Prof. Martin Ackermann's Molecular Microbial Ecology group based at Eawag (in Zurich). I have a PhD in Microbial Ecology and Evolution from the University of Oxford, where I worked with Prof. Angus Buckling, investigating how different ecological conditions can affect the evolution of anti-competitor toxins in bacteria and how this can affect bacterial virulence. My research interests are pretty varied, but in general they centre on the evolution and ecology of bacterial interactions, such as the production of anti-competitor toxins and the secretion of compounds that can be considered public goods.

Publications

• Inglis, R. F., Garfjeld Roberts, P., Gardner, A., Buckling, A. 2011. Spite and the scale of competition in Pseudomonas aeruginosa. American Naturalist 178:276-285. Link and featured on Faculty of 1000 and ScienceDaily.com
• Racey, D., R. F. Inglis, F. Harrison, A. Oliver, and A. Buckling. 2010. The effect of elevated mutation rates on the evolution of cooperation and virulence of Pseudomonas aeruginosa. Evolution 64:515–521. Link
• Inglis, R. F., A. Gardner, P. Cornelis, and A. Buckling. 2009. Spite and virulence in the bacterium Pseudomonas aeruginosa. Proceedings of the National Academy of Sciences of the United States of America 106:5703-5707. Link
• Brown, S. P., R. F. Inglis, and F. Taddei. 2009. Evolutionary ecology of microbial wars: with-in host competition and (incidental) virulence. Evolutionary Applications 2:32. Link

CV

• 2011-present ETH Postdoctoral Fellow, ETH Zurich
• 2010-2011 Postdoctoral Research Assistant, University of Oxford
• 2006-2010 DPhil Zoology, University of Oxford
• 2003-2006 BA Hons, Biological Sciences, University of Oxford

Current Research Projects

Microbial Cooperation In Biofilms:

The cellular environment plays an influential role in determining interactions between cells. Bacterial biofilms are one important example where cellular interactions and spatial association are crucial. Many bacteria produce extracellular, shared components, for example siderophores, known as public-goods. Growth in a biofilm may allow cells that engage in public-goods production to form stable mutualisms and exclude cells that do not contribute. These predictions remain theoretical and have little experimental support. To address the role that the cellular environment and spatial association plays in the maintenance of cooperative interactions in bacteria, I am conducting single-cell time-lapse experiments to study the cooperative production of siderophores in biofilms of Pseudomonas aeruginosa. I am currently constructing strains whose siderophore production can be interrupted, and in which the contribution to this public-goods can be measured at the single cell level. With this system, we hope to quantitatively describe how the growth dynamics of producers and non-producers depends on the cellular context, and to analyze how the cellular context affects the expression of siderophore genes. The goal of these experiments is to help us understand the cellular dynamics underlying cooperation in biofilms, and can give fundamental insights into biofilm formation and potential virulence determinants in infections.

Bacteriocin "Addiction Complexes":

Bacteriocin production is ubiquitous amongst bacteria. By producing proteinaceous anti-competitor toxins bacteria are able to outcompete closely related strains inhabiting similar ecological niches. In many cases (especially E. coli) these toxins are found on plasmids with closely linked immunity genes. However this presents a dilemma for bacteria, as under many conditions the bacteriocin they produce has no impact on competing bacterial strains. This leads to the prediction that the plasmid should eventually be lost as it provides no direct benefit and is in fact maladaptive. If a cell were to lose the plasmid, it would no longer produce the immunity compound and would be killed by its clone mates that are producing the toxin. So, in this respect plasmid borne bacteriocins can be considered "addiction complexes" as once a cell acquires this type of plasmid it is extremely hard to lose (mirroring other post-segregational killing mechanisms). We are currently performing experiments in the lab investigating bacteriocin plasmids and loss rates under different ecological conditions.