Figure 2.

Cellular response to PMKT exposure deduced from the analysis of the transcriptional response of S. cerevisiae to the toxin. Once PMKT has reached the cell wall through an interaction with (1→6)-β-d-glucans, PMKT interacts with the cytoplasmic membrane through the interaction with cwp2p (not shown in the figure). This interaction, through a mechanism of unknown nature (?), leads to disruption of electrochemical gradients. Cellular receptors are not included in the scheme for simplification. PMKT cause the formation of unregulated channels through which cations and small metabolites (e.g., K⁺, H⁺, Na⁺, glycerol) flow. These changes in pH_i, turgor or ionic concentrations generates a transcriptional response through the activation of Hog1p. Genes (CTT1, HSP12, HSP26, and DDR2), related with a general stress response, and genes (GPD1 and GPP2), involved in glycerol synthesis, are transcribed to compensate the toxic effects of PMKT. Cations and glycerol, among others, can leak out from sensitive cells generating cell death. Highlighted in a box are the induction levels of the most up-regulated genes. Abbreviations: DHAP (dihydroxyacetone phosphate), G3P (glycerol-3-phosphate), FBP (fructose-1,6-bisphosphate), MG (methylglyoxal), CoQ (coenzyme Q), S-LG (S-d-lactoylglutathione), GSH (glutathione).