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Published online 1 June 2004. doi:10.1083/jcb.200309097
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 165, Number 5, 653-662
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Article

 Ionophore-resistant mutant of Toxoplasma gondii reveals involvement of a sodium/hydrogen exchanger in calcium regulation

Gustavo Arrizabalaga1, Felix Ruiz2, Silvia Moreno2, and John C. Boothroyd1

1 Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305
2 Laboratory of Molecular Parasitology and Center for Zoonoses Research, Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, IL 61802

Address correspondence to John C. Boothroyd, Dept. of Microbiology and Immunology, Fairchild Building D305, 300 Pasteur Dr., Stanford University School of Medicine, Stanford, CA 94305-5124. Tel.: (650) 723-7984. Fax: (650) 723-6853. email: john.boothroyd{at}stanford.edu

Calcium is a critical mediator of many intracellular processes in eukaryotic cells. In the obligate intracellular parasite Toxoplasma gondii, for example, a rise in [Ca2+] is associated with significant morphological changes and rapid egress from host cells. To understand the mechanisms behind such dramatic effects, we isolated a mutant that is altered in its responses to the Ca2+ ionophore A23187 and found the affected gene encodes a homologue of Na+/H+ exchangers (NHEs) located on the parasite's plasma membrane. We show that in the absence of TgNHE1, Toxoplasma is resistant to ionophore-induced egress and extracellular death and amiloride-induced proton efflux inhibition. In addition, the mutant has increased levels of intracellular Ca2+, which explains its decreased sensitivity to A23187. These results provide direct genetic evidence of a role for NHE1 in Ca2+ homeostasis and important insight into how this ubiquitous pathogen senses and responds to changes in its environment.

Key Words: Toxoplasma; ionophore; egress; calcium; NHE

Abbreviations used in this paper: DMA, dimethylamiloride; HFF, human foreskin fibroblast; IID, ionophore-induced death; IIE, ionophore-induced egress; MPA, mycophenolic acid; NHE, Na+/H+ exchanger; pHe, extracellular pH; pHi, intraparasitic pH; TM, transmembrane.


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