A single Na+-Pi cotransporter in Toxoplasma plays key roles in phosphate import and control of parasite osmoregulation
Fig 14
Hypothetical model for ion homeostasis and osmoregulation in Toxoplasma.
Na+ homeostasis in Toxoplasma is accomplished via cooperation between ATP4, TgNHE1 and TgPiT. When intake of Na+ is reduced through TgPiT ablation, compensatory mechanisms may include decreased activity of ATP4 (dashed arrows) and increased activity of TgNHE1 (thick arrows), both resulting in reduced H+ concentrations in the parasite and thus cytosolic alkalinization. Consequently, the mutant decreases the export of H+ mediated by V-H+-ATPase (dashed lines). ΔTgPiT parasites have a severe constitutive loss in cytosolic ionic strength through reduced internalization of Pi and sodium into the parasite and impaired expulsion of these ions from VAC into the cytosol. Due to low Pi availability, the mutant has reduced concentrations of total Pi and polyP that is compensated for increased numbers of acidocalcisomes in an attempt to garner as much phosphate as possible.