Involvement of calcium and calmodulin in Toxoplasma gondii tachyzoite invasion
Pezzella, N.; Bouchot, A.; Bonhomme, A.; Pingret, L.; Klein, C.; Burlet, H.; Balossier, G.; Bonhomme, P.; Pinon, J.M.
European Journal of Cell Biology 74(1): 92-101
1997
ISSN/ISBN: 0171-9335 PMID: 9309395 Document Number: 480527
The tachyzoite of Toxoplasma gondii must successfully invade a host cell before it can replicate. Depletion of the Ca-2+ in the external medium (EGTA) reduced tachyzoite invasion, suggesting that the initial tachyzoite-host cell interaction is Ca-2+ dependent. The interaction of tachyzoites with host cells was also inhibited by Ca-2+ channel blockers (verapamil) and calmodulin antagonists (trifluoperazine, calmidazolium). The calmodulin concentrated at the apical end of the tachyzoite could be involved in cytoskeleton movement and conoid extrusion. Invasion also depends on changes in tachyzoite cytosolic calcium. Depletion of Ca-2+ with A23187+EGTA and release of Ca-2+ from intratachyzoite pools (nuclear and perinuclear areas) inhibited invasion. In contrast, Ca-ionophore and thapsigargin which increase host cell cytosolic Ca-2+, significantly decreased tachyzoite invasion. We therefore suggest that the effect of the drug is significantly different from the localized Ca-2+ signal that is produced after parasite attachment to its host cell receptors and leads to its internalization into the host cell.