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Calcium entry in Toxoplasma gondii and its enhancing effect of invasion-linked traits.


ABSTRACT: During invasion and egress from their host cells, Apicomplexan parasites face sharp changes in the surrounding calcium ion (Ca(2+)) concentration. Our work with Toxoplasma gondii provides evidence for Ca(2+) influx from the extracellular milieu leading to cytosolic Ca(2+) increase and enhancement of virulence traits, such as gliding motility, conoid extrusion, microneme secretion, and host cell invasion. Assays of Mn(2+) and Ba(2+) uptake do not support a canonical store-regulated Ca(2+) entry mechanism. Ca(2+) entry was blocked by the L-type Ca(2+) channel inhibitor nifedipine and stimulated by the increase in cytosolic Ca(2+) and by the specific L-type Ca(2+) channel agonist Bay K-8644. Our results demonstrate that Ca(2+) entry is critical for parasite virulence. We propose a regulated Ca(2+) entry mechanism activated by cytosolic Ca(2+) that has an enhancing effect on invasion-linked traits.

SUBMITTER: Pace DA 

PROVIDER: S-EPMC4094074 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature

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Calcium entry in Toxoplasma gondii and its enhancing effect of invasion-linked traits.

Pace Douglas A DA   McKnight Ciara A CA   Liu Jing J   Jimenez Veronica V   Moreno Silvia N J SN  

The Journal of biological chemistry 20140527 28


During invasion and egress from their host cells, Apicomplexan parasites face sharp changes in the surrounding calcium ion (Ca(2+)) concentration. Our work with Toxoplasma gondii provides evidence for Ca(2+) influx from the extracellular milieu leading to cytosolic Ca(2+) increase and enhancement of virulence traits, such as gliding motility, conoid extrusion, microneme secretion, and host cell invasion. Assays of Mn(2+) and Ba(2+) uptake do not support a canonical store-regulated Ca(2+) entry m  ...[more]

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