{"title":"铁转运体转铁蛋白1介导黑腹果蝇与普氏螺浆虫内共生关系的平衡。","authors":"Alice Marra, Florent Masson, Bruno Lemaitre","doi":"10.1093/femsml/uqab008","DOIUrl":null,"url":null,"abstract":"<p><p>Iron is involved in numerous biological processes in both prokaryotes and eukaryotes and is therefore subject to a tug-of-war between host and microbes upon pathogenic infections. In the fruit fly <i>Drosophila melanogaster</i>, the iron transporter Transferrin 1 (Tsf1) mediates iron relocation from the hemolymph to the fat body upon infection as part of the nutritional immune response. The sequestration of iron in the fat body renders it less available for pathogens, hence limiting their proliferation and enhancing the host ability to fight the infection. Here we investigate the interaction between host iron homeostasis and <i>Spiroplasma poulsonii</i>, a facultative, vertically transmitted, endosymbiont of <i>Drosophila</i>. This low-pathogenicity bacterium is devoid of cell wall and is able to thrive in the host hemolymph without triggering pathogen-responsive canonical immune pathways. However, hemolymph proteomics revealed an enrichment of Tsf1 in infected flies. We find that <i>S. poulsonii</i> induces <i>tsf1</i> expression and triggers an iron sequestration response similarly to pathogenic bacteria. We next demonstrate that free iron cannot be used by <i>Spiroplasma</i> while Tsf1-bound iron promotes bacterial growth, underlining the adaptation of <i>Spiroplasma</i> to the intra-host lifestyle where iron is mostly protein-bound. Our results show that Tsf1 is used both by the fly to sequester iron and by <i>Spiroplasma</i> to forage host iron, making it a central protein in endosymbiotic homeostasis.</p>","PeriodicalId":74189,"journal":{"name":"microLife","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2021-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10117857/pdf/","citationCount":"0","resultStr":"{\"title\":\"The iron transporter Transferrin 1 mediates homeostasis of the endosymbiotic relationship between <i>Drosophila melanogaster</i> and <i>Spiroplasma poulsonii</i>.\",\"authors\":\"Alice Marra, Florent Masson, Bruno Lemaitre\",\"doi\":\"10.1093/femsml/uqab008\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Iron is involved in numerous biological processes in both prokaryotes and eukaryotes and is therefore subject to a tug-of-war between host and microbes upon pathogenic infections. In the fruit fly <i>Drosophila melanogaster</i>, the iron transporter Transferrin 1 (Tsf1) mediates iron relocation from the hemolymph to the fat body upon infection as part of the nutritional immune response. The sequestration of iron in the fat body renders it less available for pathogens, hence limiting their proliferation and enhancing the host ability to fight the infection. Here we investigate the interaction between host iron homeostasis and <i>Spiroplasma poulsonii</i>, a facultative, vertically transmitted, endosymbiont of <i>Drosophila</i>. This low-pathogenicity bacterium is devoid of cell wall and is able to thrive in the host hemolymph without triggering pathogen-responsive canonical immune pathways. However, hemolymph proteomics revealed an enrichment of Tsf1 in infected flies. We find that <i>S. poulsonii</i> induces <i>tsf1</i> expression and triggers an iron sequestration response similarly to pathogenic bacteria. We next demonstrate that free iron cannot be used by <i>Spiroplasma</i> while Tsf1-bound iron promotes bacterial growth, underlining the adaptation of <i>Spiroplasma</i> to the intra-host lifestyle where iron is mostly protein-bound. Our results show that Tsf1 is used both by the fly to sequester iron and by <i>Spiroplasma</i> to forage host iron, making it a central protein in endosymbiotic homeostasis.</p>\",\"PeriodicalId\":74189,\"journal\":{\"name\":\"microLife\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2021-06-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10117857/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"microLife\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1093/femsml/uqab008\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2021/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"microLife","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/femsml/uqab008","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
铁参与了原核生物和真核生物的许多生物过程,因此在病原体感染时,宿主和微生物之间会展开拉锯战。在黑腹果蝇中,铁转运体转铁蛋白 1(Tsf1)在感染时介导铁从血淋巴转移到脂肪体,这是营养免疫反应的一部分。铁被螯合在脂肪体后,病原体就无法获得铁,从而限制了病原体的增殖,增强了宿主的抗感染能力。在这里,我们研究了宿主铁稳态与果蝇的一种垂直传播的面生内共生菌--普氏螺浆菌之间的相互作用。这种低致病性细菌没有细胞壁,能够在宿主血淋巴中茁壮成长,而不会触发病原体响应的典型免疫途径。然而,血淋巴蛋白质组学发现,受感染的苍蝇体内富含 Tsf1。我们发现 S. poulsonii 能诱导 tsf1 的表达,并引发类似于致病细菌的铁螯合反应。我们接下来证明,螺浆虫不能利用游离铁,而 Tsf1 结合的铁能促进细菌生长,这凸显了螺浆虫对宿主内生活方式的适应性,在宿主内,铁大多与蛋白质结合。我们的研究结果表明,Tsf1既能被苍蝇用来螯合铁,也能被螺原体用来觅食宿主铁,因此它是内共生平衡的核心蛋白。
The iron transporter Transferrin 1 mediates homeostasis of the endosymbiotic relationship between Drosophila melanogaster and Spiroplasma poulsonii.
Iron is involved in numerous biological processes in both prokaryotes and eukaryotes and is therefore subject to a tug-of-war between host and microbes upon pathogenic infections. In the fruit fly Drosophila melanogaster, the iron transporter Transferrin 1 (Tsf1) mediates iron relocation from the hemolymph to the fat body upon infection as part of the nutritional immune response. The sequestration of iron in the fat body renders it less available for pathogens, hence limiting their proliferation and enhancing the host ability to fight the infection. Here we investigate the interaction between host iron homeostasis and Spiroplasma poulsonii, a facultative, vertically transmitted, endosymbiont of Drosophila. This low-pathogenicity bacterium is devoid of cell wall and is able to thrive in the host hemolymph without triggering pathogen-responsive canonical immune pathways. However, hemolymph proteomics revealed an enrichment of Tsf1 in infected flies. We find that S. poulsonii induces tsf1 expression and triggers an iron sequestration response similarly to pathogenic bacteria. We next demonstrate that free iron cannot be used by Spiroplasma while Tsf1-bound iron promotes bacterial growth, underlining the adaptation of Spiroplasma to the intra-host lifestyle where iron is mostly protein-bound. Our results show that Tsf1 is used both by the fly to sequester iron and by Spiroplasma to forage host iron, making it a central protein in endosymbiotic homeostasis.