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J Cell Biol. 2004 Jun 7;165(5):653-62. Epub 2004 Jun 1.

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

Author information

1
Department of Microbiology and Immunology, Fairchild Building D305, 300 Pasteur Dr., Stanford University School of Medicine, Stanford, CA 94305-5124, USA.

Abstract

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.

PMID:
15173192
PMCID:
PMC2172388
DOI:
10.1083/jcb.200309097
[Indexed for MEDLINE]
Free PMC Article

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