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pubmed-article:15173192pubmed:abstractTextCalcium 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.lld:pubmed
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pubmed-article:15173192pubmed:authorpubmed-author:BoothroydJohn...lld:pubmed
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pubmed-article:15173192pubmed:articleTitleIonophore-resistant mutant of Toxoplasma gondii reveals involvement of a sodium/hydrogen exchanger in calcium regulation.lld:pubmed
pubmed-article:15173192pubmed:affiliationDepartment of Microbiology and Immunology, Fairchild Building D305, 300 Pasteur Dr., Stanford University School of Medicine, Stanford, CA 94305-5124, USA.lld:pubmed
pubmed-article:15173192pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:15173192pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed