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Phosphatidic acid as a limiting host metabolite for the proliferation of the microsporidium Tubulinosema ratisbonensis in Drosophila flies.
Nature Microbiology ( IF 20.5 ) Pub Date : 2019-01-28 , DOI: 10.1038/s41564-018-0344-y
Adrien Franchet 1, 2 , Sebastian Niehus 1 , Gaëtan Caravello 1 , Dominique Ferrandon 1
Nature Microbiology ( IF 20.5 ) Pub Date : 2019-01-28 , DOI: 10.1038/s41564-018-0344-y
Adrien Franchet 1, 2 , Sebastian Niehus 1 , Gaëtan Caravello 1 , Dominique Ferrandon 1
Affiliation
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Microsporidia are located at the base of the fungal evolutionary tree. They are obligate intracellular parasites and harness host metabolism to fuel their growth and proliferation. However, how the infestation of cells affects the whole organism and how the organism contributes to parasite proliferation remain poorly understood. Here, we have developed a Tubulinosema ratisbonensis systemic infection model in the genetically amenable Drosophila melanogaster host, in which parasite spores obtained in a mammalian cell culture infection system are injected into adult flies. The parasites proliferate within flies and ultimately kill their hosts. As commonly observed for microsporidia infecting insects, T. ratisbonensis preferentially grows in the fat body and ultimately depletes the host metabolic stores. We find that supplementing the fly diet with yeast does not benefit the host but the parasite, which increases its proliferation. Unexpectedly, fatty acids and not carbohydrates or amino acids are the critical components responsible for this phenomenon. Our genetic dissection of host lipid metabolism identifies a crucial compound hijacked by T. ratisbonensis: phosphatidic acid. We propose that phosphatidic acid is a limiting precursor for the synthesis of the parasite membranes and, hence, of its proliferation.
中文翻译：
磷脂酸作为限制性宿主代谢物，用于果蝇中微孢子虫 Tubulinosema ratisbonensis 的增殖。
微孢子虫位于真菌进化树的底部。它们是专性的细胞内寄生虫，利用宿主新陈代谢来促进它们的生长和增殖。然而，细胞的侵染如何影响整个生物体以及生物体如何促进寄生虫增殖仍然知之甚少。在这里，我们在遗传上顺从的黑腹果蝇宿主中开发了 Tubulinosema ratisbonensis 全身感染模型，其中在哺乳动物细胞培养感染系统中获得的寄生虫孢子被注射到成年果蝇中。寄生虫在苍蝇体内增殖并最终杀死它们的宿主。正如通常观察到的感染昆虫的微孢子虫一样，T. ratisbonensis 优先在脂肪体中生长并最终耗尽宿主的代谢储存。我们发现用酵母补充苍蝇饮食对宿主没有好处，而是寄生虫，这会增加其增殖。出乎意料的是，脂肪酸而不是碳水化合物或氨基酸是造成这种现象的关键成分。我们对宿主脂质代谢的遗传剖析确定了一种被 T. ratisbonensis 劫持的关键化合物：磷脂酸。我们提出磷脂酸是寄生虫膜合成的限制性前体，因此是其增殖的限制性前体。
更新日期：2019-01-29
中文翻译：
磷脂酸作为限制性宿主代谢物，用于果蝇中微孢子虫 Tubulinosema ratisbonensis 的增殖。
微孢子虫位于真菌进化树的底部。它们是专性的细胞内寄生虫，利用宿主新陈代谢来促进它们的生长和增殖。然而，细胞的侵染如何影响整个生物体以及生物体如何促进寄生虫增殖仍然知之甚少。在这里，我们在遗传上顺从的黑腹果蝇宿主中开发了 Tubulinosema ratisbonensis 全身感染模型，其中在哺乳动物细胞培养感染系统中获得的寄生虫孢子被注射到成年果蝇中。寄生虫在苍蝇体内增殖并最终杀死它们的宿主。正如通常观察到的感染昆虫的微孢子虫一样，T. ratisbonensis 优先在脂肪体中生长并最终耗尽宿主的代谢储存。我们发现用酵母补充苍蝇饮食对宿主没有好处，而是寄生虫，这会增加其增殖。出乎意料的是，脂肪酸而不是碳水化合物或氨基酸是造成这种现象的关键成分。我们对宿主脂质代谢的遗传剖析确定了一种被 T. ratisbonensis 劫持的关键化合物：磷脂酸。我们提出磷脂酸是寄生虫膜合成的限制性前体，因此是其增殖的限制性前体。
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