There are two types of plasmid integration into a host bacteria: Non-integrating plasmids replicate as with the top instance, whereas episomes, the lower example, can integrate into the host chromosome.
Horizontal gene transfer (HGT) plays an important role in the evolution of microorganisms like bacteria, but a lesser, though not unknown, role in multicellular organism. In bacteria, which freely share small bundles of DNA known as plasmids, even amongst unrelated species, HGT can be the means by which, in the right environment, a beneficial trait such as antibiotic resistance can spread rapidly through an entire microbiome. Plasmids are shed by bacteria into their environment where they can be picked up by other bacteria.
This was demonstrated recently by a study led by the researcher, Arthur Newbury, of the Environment and Sustainability Institute on Exeter University's Penryn Campus in Cornwall, UK. The significance of this finding is that it shows how antibiotic resistance can be spread by plasmids in waste water, for instance.
The Exeter University news release explains:
DNA molecules called plasmids – some of which protect bacteria from antibiotics – can spread rapidly through bacterial "communities" that are treated with antibiotics, new research shows.Although the main body of the teams research paper in the journal Proceedings of the National Academy of Sciences is behind a paywall, the abstract and statement of significance is available, open access, here
Plasmids are found within bacterial cells, sometimes slowing bacterial reproduction – but they can carry genes that stop antibiotics from working (called antimicrobial resistance).Very often, antimicrobial resistance isn't tied to the bacteria itself – it's encoded in plasmids they carry, and can pass on. Plasmids can jump between bacteria and, although most don't cause antimicrobial resistance, those that do make the new host instantly resistant.
These plasmids become beneficial when antibiotics are around, which is one reason why resistance can appear and spread very rapidly in hospitals.
Arthur Newbury, lead author
Environment and Sustainability Institute
Exeter University Penryn Campus, Penryn, Cornwall, UK.
The new laboratory study, by the University of Exeter, found that a plasmid that benefits one or more species spreads not just through those species but to others in the community.
Bacterial communities exist both in the environment and in the "microbiome" of individual organisms including humans.Our results suggest that exposure of microbial communities – including human microbiomes – to antibiotics could facilitate the spread of other plasmid-encoded genes, including antimicrobial resistance genes
There is massive potential for antimicrobial resistance caused by plasmids to spread in environmental settings.
Dr Dirk Sanders, co-author
Environment and Sustainability Institute
Exeter University Penryn Campus, Penryn, Cornwall, UK.
[…]
With one or more bacterial species benefitting from harbouring a plasmid, the plasmid reaches a "higher density" in the population – making it more likely to spread to other species.
In turn, this makes it more likely that a plasmid will be passed to a pathogenic (illness-causing) species in the community – even if that species has not yet been exposed to an antibiotic.
[…]
The study used a network approach – a highly effective way to examine complex situations ranging from bacterial communities to pandemics.
The team are already expanding this research, testing with more plasmids and more complex bacterial communities (including tests on how plasmids might spread in wastewater).
SignificanceJust one of the mechanism by which evolution occurs, but one that has been observed in action, giving the lie to the common creationist claim that evolution has never been observed so is just speculation with no evidential support – which of course ignores the fact that special creation has never been observed and was just a guess by primitive people from the infancy of our species from a time when they believe earth was flat, small, covered by a dome and ran on magic, much like the fictional Discworld of the Terry Pratchett fantasy novels, without the dome.
Antimicrobial resistance (AMR) poses a great challenge for modern medicine. Plasmids are important vectors of antibiotic resistance genes. Plasmids can have context-dependent effects on their hosts, generally slowing their growth rate but also providing protection from specific antibiotics and heavy metals. Thus, models that predict population densities based on interactions between species are useful for explaining plasmid dynamics. Here, we predict with a simple ecological model the properties of a host (e.g., bacteria) and symbiont (e.g., plasmid) interaction network. Using experimental microbial communities and a conjugative plasmid, we confirm our predictions that beneficial symbionts spread more widely through a microbial community and provide key experimental results for network ecologists seeking to uncover the determinants of ecological network structure.
Abstract
Antimicrobial resistance (AMR) genes are often carried on broad host range plasmids, and the spread of AMR within microbial communities will therefore depend on the structure of bacteria–plasmid networks. Empirical and theoretical studies of ecological interaction networks suggest that network structure differs between communities that are predominantly mutualistic versus antagonistic, with the former showing more generalized interactions (i.e., species interact with many others to a similar extent). This suggests that mutualistic bacteria–plasmid networks—where antibiotics are present and plasmids carry AMR genes—will be more generalized than antagonistic interactions, where plasmids do not confer benefits to their hosts. We first develop a simple theory to explain this link: fitness benefits of harboring a mutualistic symbiont promote the spread of the symbiont to other species. We find support for this theory using an experimental bacteria–symbiont (plasmid) community, where the same plasmid can be mutualistic or antagonistic depending on the presence of antibiotics. This short-term and parsimonious mechanism complements a longer-term mechanism (coevolution and stability) explaining the link between mutualistic and antagonistic interactions and network structure.
Newbury Arthur; Dawson Beth; Klümper Uli; Hesse Elze; Castledine Meaghan; Fontaine Colin; Buckling Angus; Sanders Dirk
Fitness effects of plasmids shape the structure of bacteria–plasmid interaction networks
Proceedings of the National Academy of Sciences (PNAS) 119(22) e2118361119; DOI: 10.1073/pnas.2118361119
Copyright: © 2022 The authors. Published by The National Academy of Science of the USA
Open access
Reprinted under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)
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