Calcium Entry in Toxoplasma gondii and Its Enhancing Effect of Invasion-linked Traits
Calcium Entry in Toxoplasma gondii and Its Enhancing Effect of Invasion-linked Traits
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DOI：
10.1074/jbc.m114.565390
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发表时间：
2014-07-11
影响因子：
4.8
通讯作者：
Moreno, Silvia N. J.
中科院分区：
文献类型：
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作者：
Pace, Douglas A.;McKnight, Ciara A.;Moreno, Silvia N. J.
在从宿主细胞侵入和排出的过程中，顶复门寄生虫面临周围钙离子（Ca 2+）浓度的急剧变化。我们的工作与弓形虫提供的证据，Ca 2+内流从细胞外环境导致胞质Ca 2+的增加和增强的毒力性状，如滑行运动，锥形挤出，微线分泌，和宿主细胞入侵。Mn 2+和Ba 2+摄取的测定不支持典型的钙库调节的Ca 2+进入机制。Ca 2+内流被L-型Ca 2+通道抑制剂硝苯地平阻断，并被胞浆Ca 2+增加和特异性L-型Ca 2+通道激动剂Bay K-8644刺激。我们的研究结果表明，Ca 2+进入寄生虫的毒力是至关重要的。我们提出了一个受调节的Ca 2+进入机制激活胞质Ca 2+，具有增强作用的入侵相关性状。
During invasion and egress from their host cells, Apicomplexan parasites face sharp changes in the surrounding calcium ion (Ca2+) concentration. Our work with Toxoplasma gondii provides evidence for Ca2+ influx from the extracellular milieu leading to cytosolic Ca2+ increase and enhancement of virulence traits, such as gliding motility, conoid extrusion, microneme secretion, and host cell invasion. Assays of Mn2+ and Ba2+ uptake do not support a canonical store-regulated Ca2+ entry mechanism. Ca2+ entry was blocked by the L-type Ca2+ channel inhibitor nifedipine and stimulated by the increase in cytosolic Ca2+ and by the specific L-type Ca2+ channel agonist Bay K-8644. Our results demonstrate that Ca2+ entry is critical for parasite virulence. We propose a regulated Ca2+ entry mechanism activated by cytosolic Ca2+ that has an enhancing effect on invasion-linked traits.