Why Bacteriophage Encode Exotoxins and other Virulence Factors

This study considers gene location within bacteria as a function of genetic element mobility. Our emphasis is on prophage encoding of bacterial virulence factors (VFs). At least four mechanisms potentially contribute to phage encoding of bacterial VFs: (i) Enhanced gene mobility could result in grea...

Full description

Bibliographic Details
Main Authors: Stephen T. Abedon, Jeffrey T. LeJeune
Format: Article
Language:English
Published: SAGE Publishing 2005-01-01
Series:Evolutionary Bioinformatics
Online Access:https://doi.org/10.1177/117693430500100001
_version_ 1828476209741168640
author Stephen T. Abedon
Jeffrey T. LeJeune
author_facet Stephen T. Abedon
Jeffrey T. LeJeune
author_sort Stephen T. Abedon
collection DOAJ
description This study considers gene location within bacteria as a function of genetic element mobility. Our emphasis is on prophage encoding of bacterial virulence factors (VFs). At least four mechanisms potentially contribute to phage encoding of bacterial VFs: (i) Enhanced gene mobility could result in greater VF gene representation within bacterial populations. We question, though, why certain genes but not others might benefit from this mobility. (ii) Epistatic interactions—between VF genes and phage genes that enhance VF utility to bacteria—could maintain phage genes via selection acting on individual, VF-expressing bacteria. However, is this mechanism sufficient to maintain the rest of phage genomes or, without gene co-regulation, even genetic linkage between phage and VF genes? (iii) Phage could amplify VFs during disease progression by carrying them to otherwise commensal bacteria colocated within the same environment. However, lytic phage kill bacteria, thus requiring assumptions of inclusive fitness within bacterial populations to explain retention of phage-mediated VF amplification for the sake of bacterial utility. Finally, (iv) phage-encoded VFs could enhance phage Darwinian fitness, particularly by acting as ecosystem-modifying agents. That is, VF-supplied nutrients could enhance phage growth by increasing the density or by improving the physiology of phage-susceptible bacteria. Alternatively, VF-mediated break down of diffusion-inhibiting spatial structure found within the multicellular bodies of host organisms could augment phage dissemination to new bacteria or to environments. Such phage-fitness enhancing mechanisms could apply particularly given VF expression within microbiologically heterogeneous environments, ie, ones where phage have some reasonable potential to acquire phage-susceptible bacteria.
first_indexed 2024-12-11T06:25:28Z
format Article
id doaj.art-f6c44dbfd3d44883b1f5fa3cd146498d
institution Directory Open Access Journal
issn 1176-9343
language English
last_indexed 2024-12-11T06:25:28Z
publishDate 2005-01-01
publisher SAGE Publishing
record_format Article
series Evolutionary Bioinformatics
spelling doaj.art-f6c44dbfd3d44883b1f5fa3cd146498d2022-12-22T01:17:41ZengSAGE PublishingEvolutionary Bioinformatics1176-93432005-01-01110.1177/117693430500100001Why Bacteriophage Encode Exotoxins and other Virulence FactorsStephen T. Abedon0Jeffrey T. LeJeune1Department of Microbiology, Ohio State University, Mansfield, OhioFood Animal Health Research Program, Ohio State University, Wooster, OhioThis study considers gene location within bacteria as a function of genetic element mobility. Our emphasis is on prophage encoding of bacterial virulence factors (VFs). At least four mechanisms potentially contribute to phage encoding of bacterial VFs: (i) Enhanced gene mobility could result in greater VF gene representation within bacterial populations. We question, though, why certain genes but not others might benefit from this mobility. (ii) Epistatic interactions—between VF genes and phage genes that enhance VF utility to bacteria—could maintain phage genes via selection acting on individual, VF-expressing bacteria. However, is this mechanism sufficient to maintain the rest of phage genomes or, without gene co-regulation, even genetic linkage between phage and VF genes? (iii) Phage could amplify VFs during disease progression by carrying them to otherwise commensal bacteria colocated within the same environment. However, lytic phage kill bacteria, thus requiring assumptions of inclusive fitness within bacterial populations to explain retention of phage-mediated VF amplification for the sake of bacterial utility. Finally, (iv) phage-encoded VFs could enhance phage Darwinian fitness, particularly by acting as ecosystem-modifying agents. That is, VF-supplied nutrients could enhance phage growth by increasing the density or by improving the physiology of phage-susceptible bacteria. Alternatively, VF-mediated break down of diffusion-inhibiting spatial structure found within the multicellular bodies of host organisms could augment phage dissemination to new bacteria or to environments. Such phage-fitness enhancing mechanisms could apply particularly given VF expression within microbiologically heterogeneous environments, ie, ones where phage have some reasonable potential to acquire phage-susceptible bacteria.https://doi.org/10.1177/117693430500100001
spellingShingle Stephen T. Abedon
Jeffrey T. LeJeune
Why Bacteriophage Encode Exotoxins and other Virulence Factors
Evolutionary Bioinformatics
title Why Bacteriophage Encode Exotoxins and other Virulence Factors
title_full Why Bacteriophage Encode Exotoxins and other Virulence Factors
title_fullStr Why Bacteriophage Encode Exotoxins and other Virulence Factors
title_full_unstemmed Why Bacteriophage Encode Exotoxins and other Virulence Factors
title_short Why Bacteriophage Encode Exotoxins and other Virulence Factors
title_sort why bacteriophage encode exotoxins and other virulence factors
url https://doi.org/10.1177/117693430500100001
work_keys_str_mv AT stephentabedon whybacteriophageencodeexotoxinsandothervirulencefactors
AT jeffreytlejeune whybacteriophageencodeexotoxinsandothervirulencefactors