Heinz Eva, Hacker Christian, Dean Paul, Mifsud John, Goldberg Alina V, Williams Tom A, Nakjang Sirintra, Gregory Alison, Hirt Robert P, Lucocq John M, Kunji Edmund R S, Embley T Martin
Institute for Cell and Molecular Biosciences, The Medical School, Newcastle University, Newcastle upon Tyne, United Kingdom; Department of Microbiology, Monash University, Melbourne, Victoria, Australia; Victoria Bioinformatics Consortium, Monash University, Melbourne, Victoria, Australia.
School of Medicine, University of St. Andrews, St. Andrews, United Kingdom.
PLoS Pathog. 2014 Dec 4;10(12):e1004547. doi: 10.1371/journal.ppat.1004547. eCollection 2014 Dec.
Microsporidia are obligate intracellular parasites of most animal groups including humans, but despite their significant economic and medical importance there are major gaps in our understanding of how they exploit infected host cells. We have investigated the evolution, cellular locations and substrate specificities of a family of nucleotide transport (NTT) proteins from Trachipleistophora hominis, a microsporidian isolated from an HIV/AIDS patient. Transport proteins are critical to microsporidian success because they compensate for the dramatic loss of metabolic pathways that is a hallmark of the group. Our data demonstrate that the use of plasma membrane-located nucleotide transport proteins (NTT) is a key strategy adopted by microsporidians to exploit host cells. Acquisition of an ancestral transporter gene at the base of the microsporidian radiation was followed by lineage-specific events of gene duplication, which in the case of T. hominis has generated four paralogous NTT transporters. All four T. hominis NTT proteins are located predominantly to the plasma membrane of replicating intracellular cells where they can mediate transport at the host-parasite interface. In contrast to published data for Encephalitozoon cuniculi, we found no evidence for the location for any of the T. hominis NTT transporters to its minimal mitochondria (mitosomes), consistent with lineage-specific differences in transporter and mitosome evolution. All of the T. hominis NTTs transported radiolabelled purine nucleotides (ATP, ADP, GTP and GDP) when expressed in Escherichia coli, but did not transport radiolabelled pyrimidine nucleotides. Genome analysis suggests that imported purine nucleotides could be used by T. hominis to make all of the critical purine-based building-blocks for DNA and RNA biosynthesis during parasite intracellular replication, as well as providing essential energy for parasite cellular metabolism and protein synthesis.
微孢子虫是包括人类在内的大多数动物群体的专性细胞内寄生虫,尽管它们具有重大的经济和医学重要性,但我们对它们如何利用受感染宿主细胞的了解仍存在重大空白。我们研究了来自人嗜气管孢虫(一种从艾滋病患者分离出的微孢子虫)的核苷酸转运(NTT)蛋白家族的进化、细胞定位和底物特异性。转运蛋白对微孢子虫的成功至关重要,因为它们弥补了该类群标志性的代谢途径的显著丧失。我们的数据表明,利用位于质膜的核苷酸转运蛋白(NTT)是微孢子虫利用宿主细胞的关键策略。在微孢子虫辐射的基部获得一个祖先转运蛋白基因后,接着是基因复制的谱系特异性事件,就人嗜气管孢虫而言,这产生了四个旁系同源的NTT转运蛋白。人嗜气管孢虫的所有四个NTT蛋白主要定位于复制性细胞内细胞的质膜,在那里它们可以在宿主 - 寄生虫界面介导转运。与已发表的关于兔脑炎微孢子虫的数据相反,我们没有发现人嗜气管孢虫的任何NTT转运蛋白定位于其最小线粒体(线粒体)的证据,这与转运蛋白和线粒体进化中的谱系特异性差异一致。当在大肠杆菌中表达时,人嗜气管孢虫的所有NTT都转运放射性标记的嘌呤核苷酸(ATP、ADP、GTP和GDP),但不转运放射性标记的嘧啶核苷酸。基因组分析表明,人嗜气管孢虫可以利用导入的嘌呤核苷酸在寄生虫细胞内复制期间制造用于DNA和RNA生物合成的所有关键嘌呤基构建块,以及为寄生虫细胞代谢和蛋白质合成提供必需的能量。