The loss of cytoplasmic potassium upon host cell breakdown triggers egress of Toxoplasma gondii
The loss of cytoplasmic potassium upon host cell breakdown triggers egress of Toxoplasma gondii
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DOI：
10.1074/jbc.m106154200
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发表时间：
2001-11-02
影响因子：
4.8
通讯作者：
Beckers, CJ
中科院分区：
文献类型：
--
作者：
Moudy, R;Manning, TJ;Beckers, CJ
细胞内寄生虫监测其宿主细胞活力的能力对其生存至关重要。原生动物寄生虫弓形虫主动侵入有核动物细胞并在细胞质中复制。感染后2 - 3天，充满寄生虫的宿主细胞分解，寄生虫离开以开始感染新细胞。寄生虫从宿主细胞中逸出是由宿主细胞质膜的破裂和随后的细胞质钾浓度的降低触发的。宿主细胞组成的许多其他变化似乎不能用作触发因素。宿主细胞[K+]的减少似乎激活了弓形虫中的磷脂酶C活性，这反过来又导致寄生虫细胞质[Ca 2 +]的增加。后者似乎是必要的和足够的诱导出口，缓冲细胞质Ca 2+块出口和钙离子载体规避需要减少宿主细胞[K+]和寄生虫磷脂酶C激活。[Ca 2 +]c的增加通过至少两种信号通路的激活而引起流出：蛋白激酶TgCDPK 1和钙调蛋白依赖性蛋白磷酸酶钙调神经磷酸酶。
The ability of intracellular parasites to monitor the viability of their host cells is essential for their survival. The protozoan parasite Toxoplasma gondii actively invades nucleated animal cells and replicates in their cytoplasm. Two to 3 days after infection, the parasite-filled host cell breaks down and the parasites leave to initiate infection of a new cell. Parasite egress from the host cell is triggered by rupture of the host plasma membrane and the ensuing reduction in the concentration of cytoplasmic potassium. The many other changes in host cell composition do not appear be used as triggers. The reduction in the host cell [K+] appears to activate a phospholipase C activity in Toxoplasma that, in turn, causes an increase in cytoplasmic [Ca2+] in the parasite. The latter appears to be necessary and sufficient for inducing egress, as buffering of cytoplasmic Ca2+ blocks egress and calcium ionophores circumvent the need for a reduction of host cell [K+] and parasite phospholipase C activation. The increase in [Ca2+]c brings about egress by the activation of at least two signaling pathways: the protein kinase TgCDPK1 and the calmodulin-dependent protein phosphatase calcineurin.