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Autor Thema: Viral Evasion of a Bacterial Suicide System by RNA–Based Molecular Mimicry Enables Infectious Altruism  (Gelesen 2531 mal)

Khan

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Simple description:
http://phys.org/news/2012-11-viruses-capable-outmanoeuvring-ability-bacteria.html

The original arcticle IN FULLTEXT!:
==> http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1003023

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Viral Evasion of a Bacterial Suicide System by RNA–Based Molecular Mimicry Enables Infectious Altruism

Tim R. Blower1, Terry J. Evans1, Rita Przybilski2, Peter C. Fineran2, George P. C. Salmond1*

1 Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom, 2 Department of Microbiology and Immunology, University of Otago, Dunedin, New Zealand

Abstract

Abortive infection, during which an infected bacterial cell commits altruistic suicide to destroy the replicating bacteriophage and protect the clonal population, can be mediated by toxin-antitoxin systems such as the Type III protein–RNA toxin-antitoxin system, ToxIN. A flagellum-dependent bacteriophage of the Myoviridae, ?TE, evolved rare mutants that “escaped” ToxIN-mediated abortive infection within Pectobacterium atrosepticum. Wild-type ?TE encoded a short sequence similar to the repetitive nucleotide sequence of the RNA antitoxin, ToxI, from ToxIN. The ?TE escape mutants had expanded the number of these “pseudo-ToxI” genetic repeats and, in one case, an escape phage had “hijacked” ToxI from the plasmid-borne toxIN locus, through recombination. Expression of the pseudo-ToxI repeats during ?TE infection allowed the phage to replicate, unaffected by ToxIN, through RNA–based molecular mimicry. This is the first example of a non-coding RNA encoded by a phage that evolves by selective expansion and recombination to enable viral suppression of a defensive bacterial suicide system. Furthermore, the ?TE escape phages had evolved enhanced capacity to transduce replicons expressing ToxIN, demonstrating virus-mediated horizontal transfer of genetic altruism.

Author Summary

Bacteria are under constant attack by their viral parasites, bacteriophages, which outnumber bacteria by an estimated ten-to-one. The constant selection pressure from this predation promotes the evolution and dissemination of bacterial bacteriophage-resistance mechanisms. One family of protective systems causes the infected cell to undergo premature suicide, in an altruistic move that protects the clonal population of bacteria by blocking virus replication. We identified a means by which a bacteriophage counter-evolved to avoid one such system. This system relies on two components: a toxic part to kill the cell and an antidote that holds the toxin in check until required. The bacteriophage evolved sequences encoding mimics of the cellular antidote and expressed these mimics so that it could continue replicating without becoming a victim of the host's defensive system. Furthermore, this evolved bacteriophage was able to transfer the DNA encoding the defence system to a new bacterial host. In so doing, the evolved bacteriophage may have indirectly created populations of host cells inside which it could productively replicate, while also providing the host better protection from competing predators.

Citation: Blower TR, Evans TJ, Przybilski R, Fineran PC, Salmond GPC (2012) Viral Evasion of a Bacterial Suicide System by RNA–Based Molecular Mimicry Enables Infectious Altruism. PLoS Genet 8(10): e1003023. doi:10.1371/journal.pgen.1003023

Editor: Josep Casadesús, Universidad de Sevilla, Spain

Received: July 3, 2012; Accepted: August 27, 2012; Published: October 18, 2012

Copyright: © Blower et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: This work was supported by grants from the Biotechnology and Biological Sciences Research Council (UK) and the Marsden Fund, Royal Society of New Zealand. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

* E-mail: gpcs@mole.bio.cam.ac.uk
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Let us hope that this will lead to find a way to do the opposite: force cancer cells into suicide.
Gespeichert