（图片来源：Jennifer Gordon and Wandy Beatty）
生物谷报道：作为单细胞的原始生物，原生动物多少有些奇特之处：它们有的像动物，有的像植物，有的兼而有之。美国科学家的一项最新研究表明，一种更像动物的原生寄生虫居然拥有一个典型的植物生物化学路径。这一结果有望为抵御由寄生虫导致的疾病（比如疟疾）开辟一条新的道路。相关论文发表在1月10日的《自然》杂志上。
由于原生寄生虫类似动物的生物学机制和宿主的十分相似，它们很难被控制。也正因为如此，许多针对这些寄生虫的药物往往会损害患者自身的细胞。
为了能够在这一问题上取得进展，美国华盛顿大学医学院的微生物学家Kisaburo Nagamune和L. David Sibley领导的研究小组对一种名为弓形虫（Toxoplasma gondii，能够导致弓形虫病）的原生动物进行了深入研究。研究人员对破译该寄生虫的沟通机制尤其感兴趣。
首先，研究人员将从弓形虫中鉴定出的生化路径与动物体内的进行了对比，以期更好地了解它们的功能。Sibley说，“当发现二者之间鲜有相似性时，我们就意识到这些原生体可能并非它们看起来的那样像动物。”
因此，研究小组将弓形虫的信号路径又与植物进行了对比，结果发现二者有许多共同点。其中最引人注目的是脱落酸（abscisic acid），一种植物体内控制应激响应和休眠的荷尔蒙。通常当宿主细胞内的弓形虫达到一定数量时，它们就会外出肆虐，而当研究人员利用一种常用的除草剂阻断弓形虫制造脱落酸后，即使数量已经足够，它们仍然保持一种无活动停滞状态。
究其原因，研究人员认为，应该是脱落酸控制着寄生虫由休眠向活跃的转变，这与植物体内的机制比较相似。进一步的研究发现，这种除草剂能够挽救被弓形虫感染的小鼠。
英国格拉斯哥大学的微生物学家Andy Waters表示，新的研究创造性地反思了包括变形虫在内的一类寄生虫，而对脱落酸角色的进一步的研究有望催生治疗疟疾急需的新方法。（科学网 任霄鹏／编译）
生物谷推荐英文原文：
Nature 451, 207-210 (10 January 2008) | doi:10.1038/nature06478; Received 2 October 2007; Accepted 13 November 2007
Abscisic acid controls calcium-dependent egress and development in Toxoplasma gondii
Kisaburo Nagamune1,4, Leslie M. Hicks2, Blima Fux1, Fabien Brossier1,4, Eduardo N. Chini3 & L. David Sibley1
Department of Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Avenue, St Louis, Missouri 63110, USA
Donald Danforth Plant Science Center, 975 N. Warson Road, St Louis, Missouri 63132, USA
Department of Anesthesiology, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA
Present addresses: Department of Immunoregulation, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan (K.N.); Linstitut National de la Researche Agronomique, Centre de Recherche de Tours, 37380 Nouzilly, France (F.B.).
Correspondence to: L. David Sibley1 Correspondence and requests for materials should be addressed to L.D.S. (Email: sibley@wustl.edu).
Abstract
Calcium controls a number of critical events, including motility, secretion, cell invasion and egress by apicomplexan parasites1. Compared to animal2 and plant cells3, the molecular mechanisms that govern calcium signalling in parasites are poorly understood. Here we show that the production of the phytohormone abscisic acid (ABA) controls calcium signalling within the apicomplexan parasite Toxoplasma gondii, an opportunistic human pathogen. In plants, ABA controls a number of important events, including environmental stress responses, embryo development and seed dormancy4, 5. ABA induces production of the second-messenger cyclic ADP ribose (cADPR), which controls release of intracellular calcium stores in plants6. cADPR also controls intracellular calcium release in the protozoan parasite T. gondii 7, 8; however, previous studies have not revealed the molecular basis of this pathway9. We found that addition of exogenous ABA induced formation of cADPR in T. gondii, stimulated calcium-dependent protein secretion, and induced parasite egress from the infected host cell in a density-dependent manner. Production of endogenous ABA within the parasite was confirmed by purification (using high-performance liquid chromatography) and analysis (by gas chromatography-mass spectrometry). Selective disruption of ABA synthesis by the inhibitor fluridone delayed egress and induced development of the slow-growing, dormant cyst stage of the parasite. Thus, ABA-mediated calcium signalling controls the decision between lytic and chronic stage growth, a developmental switch that is central in pathogenesis and transmission. The pathway for ABA production was probably acquired with an algal endosymbiont that was retained as a non-photosynthetic plastid known as the apicoplast. The plant-like nature of this pathway may be exploited therapeutically, as shown by the ability of a specific inhibitor of ABA synthesis to prevent toxoplasmosis in the mouse model.
