A simple biology experiment demonstrates the role of selection pressure in the evolution of Triclosan (a common antibiotic) resistance in Escherichia coli K12 (2). In the experiment a spread plate is made and a Triclosan soaked wafer is placed in the center – this creates a radially emanating gradual chemical gradient of Triclosan (see figure). The bacteria grow up with a Zone Of Inhibition (ZOI) surrounding the wafer, colonies on the edge of ZOI are used to inoculate the next spread plate generation, this inoculum has a population with greater resistance because the selective pressure of the higher Triclosan concentration at that location selects for resistance to this antibiotic. Where originally only a small portion of the population was resistant, successive generation lead to a plate with no measurable ZOI and sample population under high selective pressure for Triclosan resistance (sample 4 in Figure) has nearly 100% resistance (2). On a protein level Triclosan’s mode of action is binding to deactivation the enzyme FabI – an enoyl-acyl carrier protein reductase (ENR) – a ubiquitous and conserved enzyme used in fatty acid synthesis by many bacteria (3). Other ENR’s exist that are resistant to Triclosan’s action such as FabK (3). In the E. coli experiment, the selective pressure of the antibiotic selected for variants that had an ENR that was less sensitive to Triclosan binding.
1. Boyd, E. S., Anbar, A. D., Miller, S., Hamilton, T. L., Lavin, M., & Peters, J. W. (2011). A late methanogen origin for molybdenum‐dependent nitrogenase. Geobiology, 9(3), 221-232.
2. Welden, C. W., & Hossler, R. A. (2003). Evolution in the lab: biocide resistance in E. coli. The American Biology Teacher, 65(1), 56-62.
3. Heath, R. J., & Rock, C. O. (2000). Erratum: A triclosan-resistant bacterial enzyme. Nature, 406(6792), 145–146. doi:10.1038/35018162
