Vibrio cholerae
One of the mysteries of microbiology and epidemiology, is why a virulent strain of Vibrio cholerae (the bacterium that causes cholera) has remained so stable ever since it emerged in 1961 in Indonesia, causing the seventh global cholera pandemic. this strain, known as 7PET, is now the predominant strain, out-competing the other strains and infecting an estimated 1.3 - 4 million people a year, of which between 21,000 and 143,000 die.
The reason for those wide-ranging estimates is because many of the deaths from cholera are in remoter areas of mostly third-world countries where sanitation is poor, health-care is hard to obtain, and many of the victims are children, so the cause of death is often not known with any certainty.
The traditional response of creationists to anything concerning the evolution of parasites like V. cholerae is to blame 'Sin'. The more sophisticated creationists who have realised that this is a blasphemy because it implies the existence of another creator over which their supposedly omnipotent, omni-benevolent god is powerless, so they simply blame this 'sin' thing for allowing 'genetic entropy' to cause an organism to 'devolve' (it would be a serious blasphemy to call it 'evolution' so Michael J Behe and the Deception Institute had put their heads together and come up with the term 'devolution' instead, which makes it look like the exact opposite of 'evolution'. Stupidly, this devise claims that everything was created perfectly and, when Adam & Eve 'sinned', somehow this opened the door to 'sin', which apparently took their 'omniscient' god by surprise, even though it had given its alleged creations immune systems in anticipation of the effects of 'Sin'.
But of course, we can dismiss that half-baked notion which no serious biomedical scientist would take seriously because there is no mechanism for a deleterious (i.e, 'devolutionarly' trait to accumulate in the species gene pool, and whatever it is about V. cholerae that gives it the edge over other strains, can't rationally be described as 'devolutionary', or a move away from some notional initial perfection, because there can't be anything better than perfect, and yet the 7PET strain of V. cholerae is better at doing the two things it appears to have been designed to do - making more people sick and making more copies of itself than the other strains.
Explain bacterial plasmids and why they can be detrimental to the bacterium that picks them up. Bacterial plasmids are small, circular, double-stranded DNA molecules that are distinct from the chromosomal DNA of bacteria. They replicate independently of the bacterial chromosome and can be transferred between bacteria through processes such as conjugation, transformation, or transduction. Plasmids often carry genes that can provide beneficial traits to bacteria, such as antibiotic resistance, virulence factors, or metabolic pathways that enable the utilization of unusual nutrients.What exactly this trait that gives V. cholerae the competitive edge is was the discovery of a research team from The University of Texas at Austin, who have discovered that the 7PET strain is uniquely able to resist and destroy plasmids. Plasmids are small pieces of DNA that act in some ways like viruses that can infect bacteria. They can also be regarded as a simple form of sexual reproduction in that they can be passed from one bacterial cell to another, carrying genetic information. The difference being that the donor and recipient don't need to be from the same species.
However, plasmids can also be detrimental to the bacteria that acquire them for several reasons:In summary, while plasmids can confer beneficial traits to bacteria, they can also be detrimental by imposing metabolic burdens, slowing growth rates, increasing susceptibility to environmental stresses, causing genetic instability, and spreading potentially harmful genetic elements. The overall impact of a plasmid on a bacterium depends on the specific genes carried by the plasmid and the environmental context in which the bacterium finds itself.
- Metabolic Burden: Plasmids require the bacterial cell to expend energy and resources for their replication and maintenance. This can create a metabolic burden, particularly if the plasmid carries genes that are not essential for the bacteria's immediate survival or if the bacteria are in an environment where the plasmid-conferred traits do not provide a selective advantage.
- Gene Expression Costs: The expression of plasmid-encoded genes can further strain the bacterial cell's resources. Producing additional proteins, especially if they are not needed, can divert resources away from essential cellular processes, reducing the bacterium's overall fitness.
- Reduced Growth Rate: Due to the additional metabolic burden and resource allocation for plasmid replication and gene expression, plasmid-carrying bacteria often exhibit slower growth rates compared to plasmid-free counterparts. In competitive environments, this can place plasmid-bearing bacteria at a disadvantage.
- Increased Susceptibility to Environmental Stresses: The metabolic burden imposed by plasmids can make bacteria more susceptible to environmental stresses, such as nutrient limitation or changes in temperature and pH. The additional energy required to maintain and express plasmid genes can reduce the bacteria's ability to cope with these stresses.
- Potential for Genetic Instability: Some plasmids can cause genetic instability in the host bacterium. This can occur through mechanisms such as plasmid integration into the chromosomal DNA, disruption of essential genes, or promoting the spread of other mobile genetic elements, which can lead to detrimental genetic changes.
- Horizontal Gene Transfer Risks: While horizontal gene transfer (HGT) can spread beneficial traits rapidly through bacterial populations, it can also spread deleterious or redundant plasmids. Bacteria that acquire plasmids without beneficial genes may end up carrying an unnecessary genetic load, which can negatively impact their fitness.
Should plasmids be regarded as parasites?
The classification of plasmids as parasites is nuanced and depends on the context of their relationship with their bacterial hosts. Here’s a detailed examination:
Parasitic Characteristics of Plasmids
Mutualistic Characteristics of Plasmids
- Resource Utilization: Plasmids consume the host's resources for their replication and maintenance, which can impose a metabolic burden on the host. This relationship resembles parasitism, where one organism (the plasmid) benefits at the expense of another (the host bacterium).
- Reduced Host Fitness: In some cases, the presence of a plasmid can reduce the host bacterium's fitness, leading to slower growth rates and increased vulnerability to environmental stresses. This detrimental impact on the host's fitness aligns with the parasitic nature of taking resources without providing immediate benefits.
Context-Dependent Nature
- Beneficial Traits: Many plasmids carry genes that provide significant advantages to the host, such as antibiotic resistance, virulence factors, or metabolic pathways that enhance survival under specific conditions. This mutualistic aspect suggests a symbiotic relationship where both the plasmid and the host benefit.
- Adaptive Advantage: In certain environments, the traits conferred by plasmid genes can provide a selective advantage, enhancing the host’s survival and proliferation. For instance, in the presence of antibiotics, plasmids carrying resistance genes can enable the host to survive and reproduce, thereby ensuring the plasmid’s propagation.
The relationship between plasmids and their bacterial hosts can be highly context-dependent:Evolutionary Perspective
- In Non-Stressful Environments: In the absence of selective pressures, such as antibiotics, the metabolic burden of carrying a plasmid might outweigh any potential benefits, making the plasmid more parasitic.
- Under Selective Pressure: When environmental conditions favor the traits conferred by plasmid genes, the plasmid can be highly beneficial, fostering a mutualistic relationship.
From an evolutionary standpoint, plasmids can be seen as elements that enhance genetic diversity and adaptability in bacterial populations. They enable rapid acquisition and dissemination of advantageous traits, which can be crucial for survival in changing environments.
Conclusion
Plasmids can exhibit both parasitic and mutualistic characteristics, and their classification depends on the specific interactions and environmental context. In scenarios where the plasmid imposes a significant metabolic burden without providing immediate benefits, it acts more like a parasite. Conversely, when the plasmid confers advantageous traits that improve host survival, it fosters a mutualistic relationship. Thus, rather than fitting neatly into the category of parasites, plasmids are better understood as flexible genetic elements that can shift between parasitism and mutualism depending on the circumstances.
But, although plasmids can carry information to give, for example, antibiotic resistance, they can also be detrimental to the host, wasting energy to replicate them and inserting themselves in the genome, causing detrimental mutations. Plasmids are a major environmental driver of bacterial evolution.
7PET has the ability to detect and destroy plasmids, so avoiding the detrimental effects of them and consequently remaining relatively stable over time.
How the University of Texas team discovered this is the subject of a University of Texas at Austin news release:
A deadly strain of cholera bacteria that emerged in Indonesia back in 1961 continues to spread widely to this day, claiming thousands of lives around the world every year, sickening millions — and, with its persistence, baffling scientists. Finally, in a study published yesterday in Nature, researchers from The University of Texas at Austin have discovered how this dangerous strain has held out over decades.The team's paper in Nature is an unedited version published ahead of the publication which will require further editing. Sadly, we only have the abstract as the full paper is behind an expensive paywall:
A longstanding mystery about the strain of Vibrio cholerae (V. cholerae) responsible for the seventh global cholera pandemic is how this lineage has managed to out-compete other pathogenic variants. The UT team identified a unique quirk of the immune system that protects the bacteria from a key driver of bacterial evolution.
This component of the immune system is unique to this strain, and it has likely given it an extraordinary advantage over other V. Cholerae lineages. It has also allowed it to defend against parasitic mobile genetic elements, which has likely played a key part in the ecology and evolution of this strain and ultimately contributed to the longevity of this pandemic lineage.
Dr Jack P. K. Bravo, corresponding author. Department of Molecular Biosciences
University of Texas at Austin, Austin, Texas, USA
Cholera and other bacteria, like all living things, evolve through a series of mutations and adaptations over time, allowing for new developments in a changing environment, such as antibiotic resistance. Some of the drivers of evolution in microbes are even smaller DNA structures called plasmids that infect, exist and replicate inside a bacterium in ways that can change bacterial DNA. Plasmids also can use up energy and cause mutations that are less advantageous for the bacteria.
Through a combination of laboratory analysis and cryo-electron-microscope imaging, the research team identified a unique two-part defense system that these bacteria have that essentially destroys plasmids, thus protecting and preserving the bacterial strain.
The World Health Organization estimates that cholera infects 1.3 million to 4 million people a year and that between 21,000 and 143,000 die annually. The bacterium is usually spread through contaminated water and food or contact with an infected person’s fluids. Severe cases are marked by diarrhea, vomiting and muscle cramps that can lead to dehydration, sometimes fatally. Outbreaks occur mostly in areas with poor sanitation and drinking water infrastructure. Although there is currently a vaccine to fight cholera, protection against severe symptoms drops after only three months. With new interventions needed, researchers say their study offers a potential new avenue for drugmakers to explore.
This unique defense system could be a target for treatment or prevention. If we can remove this defense, it could leave it vulnerable, or if we can turn its own immune system back on the bacteria, it would be an effective way to destroy it.
Associate Professor David W. Taylor, Department of Molecular Biosciences
University of Texas at Austin, Austin, Texas, USA
The defense system outlined in the paper consists of two parts that work together. One protein targets the DNA of plasmids with remarkable accuracy, and a complementary enzyme shreds the DNA of the plasmid, unwinding the helix of the DNA moving in opposite directions.
Researchers noted that this system is also similar to some of the CRISPR-Cascade complexes, which are also based on bacterial immune systems. The CRISPR discovery eventually revolutionized gene-editing technologies that have brought about massive biomedical breakthroughs.
Delisa A. Ramos, Rodrigo Fregoso Ocampo and Caiden Ingram of UT were also authors on the paper.
AbstractSince the mutation does nothing except make V. cholerae more effective at making us sick and producing more copies of itself - the definition of biological success - there is no way this can be presented as devolutionary, so we can dismiss the scientifically nonsensical notion of 'Sin' causign 'genetic entropy' which causes 'devolution' from an original perfect creation, as an explanation for this mutation in V. cholerae which means it can make even more people sick and die. This leaves creationists who still insist that evolution can't explain bacterial parasites and who believe in an omniscient designer god, with no choice; they have to accept that this virulent 7PET strain must be the work of a designer with malevolent intent.
While eukaryotic Argonautes play a pivotal role in post-transcriptional gene regulation through nucleic acid cleavage, some short prokaryotic Argonaute variants (pAgos) rely on auxiliary nuclease factors for efficient foreign DNA degradation (1). Here, we elucidate the activation pathway of the DNA Defense Module DdmDE system, which rapidly eliminates small, multicopy plasmids from Vibrio cholerae Seventh Pandemic Strain (7PET) (2). Through a combination of cryo-EM, biochemistry and in vivo plasmid clearance assays, we demonstrate DdmE is a catalytically inactive, DNA-guided, DNA-targeting pAgo with a distinctive insertion domain. We observe that DdmD transitions from an autoinhibited, dimeric protein to monomers upon loading of single-stranded DNA targets. Furthermore, the complete structure of the DdmDE-guide-target handover complex provides a comprehensive view into how DNA recognition triggers processive plasmid destruction. Our work establishes a mechanistic foundation for how pAgo utilize ancillary factors to achieve plasmid clearance, and provides insights into anti-plasmid immunity in bacteria.
Bravo, J.P.K., Ramos, D.A., Ocampo, R.F. et al.
Plasmid targeting and destruction by the DdmDE bacterial defence system. Nature (2024). https://doi.org/10.1038/s41586-024-07515-9
© 2024 Springer Nature Ltd.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.
Incidentally, to rub more salt into creationists' wounds, a perfect genome can't change even to 'devolve' because part of genetic perfection is the ability to replicate perfectly without error, yet any change from some notional perfection, either by rational 'evolution' or irrational 'devolution', requires variance produced by imperfect replication. Behe's desperate attempt to introduce Christian superstiton into biology, so it can be used as a vehicle for intruducing fundamentalist Chritianity into the school science curriculum at tax-payers' expense has resulted in a paradox that can't be resolved. Starting from perfection, there is no possible way a genome can change, so no mechanism for creating the biodiversity he set out to try to explain away.
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