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Mitochondrial dual-coding genes in Trypanosoma brucei

Trypanosoma brucei is transmitted between mammalian hosts by the tsetse fly. In the mammal, they are exclusively extracellular, continuously replicating within the bloodstream. During this stage, the mitochondrion lacks a functional electron transport chain (ETC). Successful transition to the fly, r...

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Detalles Bibliográficos
Autores principales: Kirby, Laura E., Koslowsky, Donna
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5650466/
https://www.ncbi.nlm.nih.gov/pubmed/28991908
http://dx.doi.org/10.1371/journal.pntd.0005989
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author Kirby, Laura E.
Koslowsky, Donna
author_facet Kirby, Laura E.
Koslowsky, Donna
author_sort Kirby, Laura E.
collection PubMed
description Trypanosoma brucei is transmitted between mammalian hosts by the tsetse fly. In the mammal, they are exclusively extracellular, continuously replicating within the bloodstream. During this stage, the mitochondrion lacks a functional electron transport chain (ETC). Successful transition to the fly, requires activation of the ETC and ATP synthesis via oxidative phosphorylation. This life cycle leads to a major problem: in the bloodstream, the mitochondrial genes are not under selection and are subject to genetic drift that endangers their integrity. Exacerbating this, T. brucei undergoes repeated population bottlenecks as they evade the host immune system that would create additional forces of genetic drift. These parasites possess several unique genetic features, including RNA editing of mitochondrial transcripts. RNA editing creates open reading frames by the guided insertion and deletion of U-residues within the mRNA. A major question in the field has been why this metabolically expensive system of RNA editing would evolve and persist. Here, we show that many of the edited mRNAs can alter the choice of start codon and the open reading frame by alternative editing of the 5’ end. Analyses of mutational bias indicate that six of the mitochondrial genes may be dual-coding and that RNA editing allows access to both reading frames. We hypothesize that dual-coding genes can protect genetic information by essentially hiding a non-selected gene within one that remains under selection. Thus, the complex RNA editing system found in the mitochondria of trypanosomes provides a unique molecular strategy to combat genetic drift in non-selective conditions.
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spelling pubmed-56504662017-11-03 Mitochondrial dual-coding genes in Trypanosoma brucei Kirby, Laura E. Koslowsky, Donna PLoS Negl Trop Dis Research Article Trypanosoma brucei is transmitted between mammalian hosts by the tsetse fly. In the mammal, they are exclusively extracellular, continuously replicating within the bloodstream. During this stage, the mitochondrion lacks a functional electron transport chain (ETC). Successful transition to the fly, requires activation of the ETC and ATP synthesis via oxidative phosphorylation. This life cycle leads to a major problem: in the bloodstream, the mitochondrial genes are not under selection and are subject to genetic drift that endangers their integrity. Exacerbating this, T. brucei undergoes repeated population bottlenecks as they evade the host immune system that would create additional forces of genetic drift. These parasites possess several unique genetic features, including RNA editing of mitochondrial transcripts. RNA editing creates open reading frames by the guided insertion and deletion of U-residues within the mRNA. A major question in the field has been why this metabolically expensive system of RNA editing would evolve and persist. Here, we show that many of the edited mRNAs can alter the choice of start codon and the open reading frame by alternative editing of the 5’ end. Analyses of mutational bias indicate that six of the mitochondrial genes may be dual-coding and that RNA editing allows access to both reading frames. We hypothesize that dual-coding genes can protect genetic information by essentially hiding a non-selected gene within one that remains under selection. Thus, the complex RNA editing system found in the mitochondria of trypanosomes provides a unique molecular strategy to combat genetic drift in non-selective conditions. Public Library of Science 2017-10-09 /pmc/articles/PMC5650466/ /pubmed/28991908 http://dx.doi.org/10.1371/journal.pntd.0005989 Text en © 2017 Kirby, Koslowsky http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Kirby, Laura E.
Koslowsky, Donna
Mitochondrial dual-coding genes in Trypanosoma brucei
title Mitochondrial dual-coding genes in Trypanosoma brucei
title_full Mitochondrial dual-coding genes in Trypanosoma brucei
title_fullStr Mitochondrial dual-coding genes in Trypanosoma brucei
title_full_unstemmed Mitochondrial dual-coding genes in Trypanosoma brucei
title_short Mitochondrial dual-coding genes in Trypanosoma brucei
title_sort mitochondrial dual-coding genes in trypanosoma brucei
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5650466/
https://www.ncbi.nlm.nih.gov/pubmed/28991908
http://dx.doi.org/10.1371/journal.pntd.0005989
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