Figure 8. Model of the role of TgTRPPL-2 in Ca²⁺influx into the cytosol of T. gondii.

Ca²⁺ entry is mediated by two independent Ca²⁺ channels at the PM, a nifedipine-sensitive channel (NSC) and TgTRPPL-2. TgTRPPL-2 is a cation-permeable channel that mediates Ca²⁺ entry at the PM by a pathway that is activated by high [Ca²⁺] and can be inhibited by broad transient receptor potential inhibitors like anthranilic acid and benzamil. TgA1 is shown as the PM Ca²⁺ ATPase that pumps Ca²⁺ outside the cell. TgTRPPL-2 also localizes to the endoplasmic reticulum (ER) where it may function as a Ca²⁺ efflux channel. Increase in cytosolic [Ca²⁺] can modulate TgTRPPL-2 by allowing the channel to open for longer time, thus allowing more Ca²⁺ to enter the cell. Also shown is the IP₃-responsive channel in the ER. The molecular identity of this channel is not known. Ca²⁺ activates the phosphatidyl inositol phospholipase C (PLC), which is also activated through protein kinase G signaling. PLC synthesizes IP₃, which stimulates Ca²⁺ release from the ER.