Dobrowolski J M, Sibley L D
Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri, 63110, USA.
Cell. 1996 Mar 22;84(6):933-9. doi: 10.1016/s0092-8674(00)81071-5.
Toxoplasma gondii is an obligate intracellular parasite that invades a wide range of vertebrate host cells. We demonstrate that invasion is critically dependent on actin filaments in the parasite, but not the host cell. Invasion into cytochalasin D (CD)-resistant host cells was blocked by CD, while parasite mutants invaded wild-type host cells in the presence of drug. CD resistance in Toxoplasma was mediated by a point mutation in the single-copy actin gene ACT1. Transfection of the mutant act1 allele into wild-type Toxoplasma conferred motility and invasion in the presence of CD. We conclude that host cell invasion by Toxoplasma, and likely by related Apicomplexans, is actively powered by an actin-based contractile system in the parasite.
刚地弓形虫是一种专性细胞内寄生虫，可侵入多种脊椎动物宿主细胞。我们证明，入侵严重依赖于寄生虫中的肌动蛋白丝，而不是宿主细胞中的肌动蛋白丝。侵入对细胞松弛素D（CD）有抗性的宿主细胞会被CD阻断，而寄生虫突变体在有药物存在的情况下可侵入野生型宿主细胞。弓形虫对CD的抗性是由单拷贝肌动蛋白基因ACT1中的一个点突变介导的。将突变的act1等位基因转染到野生型弓形虫中，可使其在有CD存在的情况下具有运动性和入侵能力。我们得出结论，弓形虫以及可能相关的顶复门寄生虫对宿主细胞的入侵是由寄生虫中基于肌动蛋白的收缩系统主动驱动的。
