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Specific role of mitochondrial electron transport in blood-stage Plasmodium falciparum

机译：线粒体电子传递在血液恶性疟原虫中的特殊作用

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The origin of all mitochondria can be traced to the symbiotic arrangement that resulted in the emergence of eukaryotes in a world that was exclusively populated by prokaryotes. This arrangement, however, has been in continuous genetic flux: the varying degrees of gene loss and transfer from the mitochondrial genome in different eukaryotic lineages seem to signify an ongoing 'conflict' between the host and the symbiont. Eukaryotic parasites belonging to the phylum Apicomplexa provide an excellent example to support this view. These organisms contain the smallest mitochondrial genomes known, with an organization that differs among various genera; one genus, Cryptosporidium, seems to have lost the entire mitochondrial genome. Here we show that erythro-cytic stages of the human malaria parasite Plasmodiutn falciparum seem to maintain an active mitochondrial electron transport chain to serve just one metabolic function: regeneration of ubiquinone required as the electron acceptor for dihydroorotate dehydrogen-ase, an essential enzyme for pyrimidine biosynthesis. Transgenic P. falciparum parasites expressing Saccharomyces cerevisiae dihy-droorotate dehydrogenase, which does not require ubiquinone as an electron acceptor, were completely resistant to inhibitors of mitochondrial electron transport. Maintenance of mitochondrial membrane potential, however, was essential in these parasites, as indicated by their hypersensitivity to proguanil, a drug that collapsed the membrane potential in the presence of electron transport inhibitors. Thus, acquisition of just one enzyme can render mitochondrial electron transport nonessential in erythrocytic stages of P. falciparum.
机译：所有线粒体的起源都可以追溯到共生安排，这种共生安排导致真核生物出现在一个仅由原核生物组成的世界中。然而，这种安排是连续不断的遗传变化：不同真核细胞谱系中线粒体基因组中基因丢失和转移的程度不同，似乎表明宿主与共生体之间正在进行“冲突”。属于复杂门的真核生物提供了一个很好的例子来支持这种观点。这些生物包含已知的最小的线粒体基因组，其组织在各个属之间有所不同。一个属，隐孢子虫，似乎已经失去了整个线粒体基因组。在这里，我们显示人类疟疾寄生虫恶性疟原虫的红细胞阶段似乎维持了活跃的线粒体电子传输链，仅起到一种代谢功能：泛醌的再生作为二氢乳清酸脱氢酶的电子受体所必需的，这是嘧啶的必需酶生物合成。表达酿酒酵母二氢-杜鹃花酸脱氢酶的转基因恶性疟原虫寄生虫，不需要泛醌作为电子受体，对线粒体电子运输的抑制剂具有完全的抵抗力。然而，线粒体膜电位的维持在这些寄生虫中是必不可少的，正如它们对丙胍的超敏反应所表明的那样，丙guan是一种在电子传输抑制剂的存在下使膜电位崩溃的药物。因此，仅获得一种酶就可以使恶性疟原虫的红细胞阶段线粒体电子运输不再重要。

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