Figure 5

Overview of the model. The hyperosmotic stress signal is represented as the change in the difference between intracellular and extracellular osmotic pressures (i.e.S(t) = (Π _i ⁰ − Π _e ⁰) − [Π _i (t) − Π _e (t)]; Π _i ⁰: initial intracellular osmolarity, Π _e ⁰: initial extracellular osmolarity, Π _i (t): current intracellular osmolarity, Π _e (t) current extracellular osmolarity). Thus, the initial signal is equivalent to the increase in osmolarity caused by the extracellular NaCl. Upon an increase in extracellular osmolarity, the signal becomes positive and activates an intermediate kinase (v₁) and then Hog1 (v₃), both of which are balanced by dephosphorylation activities (v₂, and v₄ respectively, associated kinetic parameters are constant). Once activated, Hog1 induces the activity of glycerol production machinery (GPM) (v₅) which produces glycerol. Intracellular glycerol passively diffuses out of the cell through an aquaglyceroporin (AGP), driven by the concentration gradient across cell membrane (v₆). Hyperosmotic shock triggers rapid closure of the aquaglyceroporin to retain glycerol, while a hypoosmotic condition causes the aquaglyceroporin to open to a higher degree than that of the steady-state (v₆) and triggers a rapid decrease in the glycerol biosynthesis rate (v₇). In both C. albicans and S. cerevisiae, increased intracellular glycerol concentration elevates the intracellular osmotic pressure and eventually attenuates the signal, indicating adaptation to the new condition.