Fig. 8

A model for IIL toxicity and resistance. We propose the model of imidazolium IIL toxicity. In the presence of IILs at near neutral pH (a), cells pump out protons via Pma1p, which is coupled with import of the [EMIM]⁺ cation that results in hyperpolerization of the mitochondrial membrane. PTK2 activates Pma1p via phosphorlaytion. Deletion of PTK2 alleviates this by reducing Pma1p activity, and thus [EMIM]Cl influx. The effects of mitochondrial perturbation are more acute in aerobic conditions (red stars vs yellow stars), where mitochondria are more active. At lower pH (b), [EMIM]Cl import is lessened, similar to the polyamine cation spermine, which is alone regulated by PTK2