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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Hamilton, Phineas T. Boulanger, Martin J. Perlman, Steve J. Peng, Fangni |
| Description | Author Affiliation: Hamilton PT ( Department of Biology, University of Victoria, Victoria, BC, Canada V8W 2Y2); Peng F ( Department of Biochemistry and Microbiology, University of Victoria, Victoria, BC, Canada V8P 5C2); Boulanger MJ ( Department of Biochemistry and Microbiology, University of Victoria, Victoria, BC, Canada V8P 5C2); Perlman SJ ( Department of Biology, University of Victoria, Victoria, BC, Canada V8W 2Y2); |
| Abstract | Vertically transmitted symbionts that protect their hosts against parasites and pathogens are well known from insects, yet the underlying mechanisms of symbiont-mediated defense are largely unclear. A striking example of an ecologically important defensive symbiosis involves the woodland fly Drosophila neotestacea, which is protected by the bacterial endosymbiont Spiroplasma when parasitized by the nematode Howardula aoronymphium. The benefit of this defense strategy has led to the rapid spread of Spiroplasma throughout the range of D. neotestacea, although the molecular basis for this protection has been unresolved. Here, we show that Spiroplasma encodes a ribosome-inactivating protein (RIP) related to Shiga-like toxins from enterohemorrhagic Escherichia coli and that Howardula ribosomal RNA (rRNA) is depurinated during Spiroplasma-mediated protection of D. neotestacea. First, we show that recombinant Spiroplasma RIP catalyzes depurination of 28S rRNAs in a cell-free assay, as well as Howardula rRNA in vitro at the canonical RIP target site within the -sarcin/ricin loop (SRL) of 28S rRNA. We then show that Howardula parasites in Spiroplasma-infected flies show a strong signal of rRNA depurination consistent with RIP-dependent modification and large decreases in the proportion of 28S rRNA intact at the -sarcin/ricin loop. Notably, host 28S rRNA is largely unaffected, suggesting targeted specificity. Collectively, our study identifies a novel RIP in an insect defensive symbiont and suggests an underlying RIP-dependent mechanism in Spiroplasma-mediated defense. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 2 |
| Volume Number | 113 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2016-01-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Drosophila Metabolism Microbiology Ribosome Inactivating Proteins Spiroplasma Physiology Symbiosis Animals Endoribonucleases Chemistry Fungal Proteins Polymerase Chain Reaction RNA, Ribosomal, 28S Rabbits Recombinant Proteins Isolation & Purification Ribosomes Ricin Sequence Analysis, RNA Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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