How the hospital pathogen Acinetobacter baumannii quickly adapts to new environmental conditions | Aktuelles aus der Goethe-Universität Frankfurt
Model of the type IVa pilus (T4aP) in A. baylyi. OM–Outer membrane; IM–Inner membrane; PG–peptidoglycan. The individual components are listed in Table 1.
From: Iruegas R, Pfefferle K, Göttig S, Averhoff B, Ebersberger I (2023)
In fact, the evolution of the bacterial flagellum by exaptation of pre-existing structures, namely the Type III secretory system that bacteria use to anchor themselves to target cells before parasitizing them, was known about before he wrote his book, as Kenneth Miller has pointed out - a fact that Behe has failed to acknowledge in subsequent editions.
Kenneth R. Miller's Refutation of Behe's Intelligent [sic] Design Argument.But hey! Why spoil a nice little earner with some inconvenient truths, when truth is the last thing your target readership is interested in? Telling the truth to creationists is not what the Discovery Institute pays its hirelings for.
Kenneth R. Miller, a biologist and professor at Brown University, provided a comprehensive response to Michael J. Behe's "irreducible complexity" argument in his testimony during the Kitzmiller v. Dover trial in 2005. Behe had argued that certain biological structures, like the bacterial flagellum, were irreducibly complex and could not have evolved through gradual, step-by-step processes.
Miller's refutation of Behe's argument was based on several key points:In summary, Kenneth Miller effectively refuted Michael J. Behe's "irreducible complexity" argument by providing detailed explanations, experimental evidence, and scientific consensus that supported the gradual evolution of complex biological systems, including the bacterial flagellum. His testimony played a significant role in the Kitzmiller v. Dover trial, which ultimately ruled against the teaching of intelligent design in public school science classes.
- Explanations for the Evolution of the Bacterial Flagellum: Miller explained that the bacterial flagellum could indeed have evolved through a series of incremental steps, each conferring a functional advantage. He provided examples of simpler systems that perform different functions and proposed a plausible pathway for the evolution of the flagellum. One such pathway involved a protein secretion system, which is structurally similar to the flagellum and serves as a precursor.
- Homologous Structures: Miller highlighted the presence of homologous structures in different organisms, which share common ancestry and have undergone modifications over time. He pointed out that several components of the bacterial flagellum are found in other structures, such as the Type III secretion system and the ATP synthase complex. These components serve different functions in various organisms, indicating a shared evolutionary history.
- Experimental Evidence: Miller presented experimental evidence of the evolution of complex systems in the laboratory. He discussed the work of researcher Barry Hall, who successfully evolved a simpler system into a more complex one over generations of bacteria. This experiment demonstrated that the step-by-step evolution of complex structures is feasible.
- Computer Simulations: Miller referenced computer simulations that showed how irreducibly complex systems could evolve. He presented the work of scientist Daniel Dykstra, who used a genetic algorithm to evolve a simulated irreducibly complex system.
- Scientific Consensus: Miller emphasized that Behe's argument was not widely accepted within the scientific community. He cited numerous scientific papers and publications that offered explanations and evidence for the evolution of complex structures, including the bacterial flagellum.
ChatGPT3 "How did Kenneth Miller refute Michael J Behe's 'irreducibly complex' argument with the bacterial flagellum?" [Response to user question]
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But what Behe inadvertently did with that book was in effect to argue that an intelligent designer is designing pathogens the better to make us sick. So, let's run with that idea for the sake of argument.
What a team of bioinformaticians led by Professor Ingo Ebersberger of Goethe University Frankfurt and the LOEWE Center for Translational Biodiversity Genomics (LOEWE-TBG) have shown is that the troublesome hospital pathogen, Acinetobacter baumannii has been ingeniously 'designed' so it doesn't matter what the receptors on your cells the bacterium needs to bind to to make you sick, one strain or another will have the required key to fit the lock, so to speak. This was achieved by modifying the protein at the tip of the structure so it's different in different strains.
The structure which has been modified is known as the type IVa (T4A) pili, a structure common to lots of different bacteria, not all of which are pathogenic. And any creationist worthy of the name would look at the T4A pili and declare it to be irreducibly complex, without further investigation, and therefore 'God did it!'.
As the Goethe University news release explains:
Hospital-acquired infections are often hard to treat because the corresponding pathogens become increasingly resistant against antibiotics. Here, the bacterium Acinetobacter baumannii is particularly feared, and there is great pressure to devise novel therapeutic approaches to combat it. Bioinformaticians from Goethe University Frankfurt and Research Unit FOR2251 of the German Research Foundation have now detected an unexpectedly wide diversity of certain cell appendages in A. baumannii that are associated with pathogenicity. This could lead to treatment strategies that are specifically tailored to a particular pathogen.
Each year, over 670,000 people in Europe fall ill because of antibiotic-resistant pathogens, and 33,000 die from the infections. Especially feared are pathogens with resistances against multiple, or even all, known antibiotics. One of these is the bacterium Acinetobacter baumannii, feared today above all as the “hospital superbug”: According to estimates, up to five percent of all hospital-acquired and one tenth of all bacterial infections resulting in death can be attributed to this pathogen alone. This puts A. baumannii right at the top of a list of pathogens for which – according to the World Health Organization (WHO) – there is an urgent need to develop new therapies.
Understanding which characteristics make A. baumannii a pathogen is one of the prerequisites for this. To this end, bioinformaticians led by Professor Ingo Ebersberger of Goethe University Frankfurt and the LOEWE Center for Translational Biodiversity Genomics (LOEWE-TBG) are comparing the genomes and the proteins encoded therein across a wide range of different Acinetobacter strains. Conclusions about which genes contribute to pathogenicity can be drawn above all from the differences between dangerous and harmless strains.
Due to a lack of suitable methods, corresponding studies have so far concentrated on whether a gene is present in a bacterial strain or not. However, this neglects the fact that bacteria can acquire new characteristics by modifying existing genes and thus also the proteins encoded by them. That is why Ebersberger’s team has developed a bioinformatics method to track the modification of proteins along an evolutionary lineage and has now applied this method for the first time to Acinetobacter in collaboration with microbiologists from the Institute for Molecular Biosciences and the Institute of Medical Microbiology and Infection Control at Goethe University Frankfurt.
In the process, the researchers concentrated on hair-like cell appendages, known as type IVa (T4A) pili, which are prevalent in bacteria and that they use to interact with their environment. The fact that they are present in harmless bacteria on the one hand and have even been identified as a key factor for the virulence of some pathogens on the other suggests that the T4A pili have repeatedly acquired new characteristics associated with pathogenicity during evolution.In this way, drastic functional modifications can be achieved over short evolutionary time spans,” Ebersberger is convinced. “We assume that bacterial strains that differ in terms of their T4A pili also interact differently with their environment. This might determine, for example, in which corner of the human body the pathogen settles.
Building on our results, it might be possible to develop personalized therapies that are tailored to a specific strain of the pathogen. Our approach has gone a long way towards resolving the search for possible components that characterize pathogens.
Professor Ingo Ebersberger, senior author
Applied Bioinformatics Group
Inst of Cell Biology and Neuroscience
Goethe University, Frankfurt am Main, Germany.
The research team could show that the protein ComC, which sits on the tip of the T4A pili and is essential for their function, shows conspicuous changes within the group of pathogenic Acinetobacter strains. Even different strains of A. baumannii have different variants of this protein. This leads bioinformatician Ebersberger to compare the T4A pili to a multifunctional garden tool, where the handle is always the same, but the attachments are interchangeable.
The aim is to use this knowledge of the unexpectedly high diversity within the pathogen to improve the treatment of A. baumannii infections. However, the study by Ebersberger and his colleagues also reveals something else: Previous studies on the comparative genomics of A. baumannii have presumably only unveiled the tip of the iceberg.
As though that weren't bad enough for creationists, the authors leave no doubt at all that they understand this as an evolutionary process and show no indication that the TOE might not be adequate for the purpose of explaining the observations:
AbstractThen there is that other little problem for creationists: when they are confronted with, using their own arguments, that it would men their beloved creator god is deliberately creating ways to make us sick and to combat advances medical science is making with antibiotics, they have to abandon the pretense of science, resort to religious superstition and blame 'sin' which entered the world with The Fall', so destroying the intelligent [sic] design argument for their god, based on 'irreducibly complex' pathogens like E. coli and this one, A. baumannii.
The Gram-negative bacterial pathogen Acinetobacter baumannii is a major cause of hospital-acquired opportunistic infections. The increasing spread of pan-drug resistant strains makes A. baumannii top-ranking among the ESKAPE pathogens for which novel routes of treatment are urgently needed. Comparative genomics approaches have successfully identified genetic changes coinciding with the emergence of pathogenicity in Acinetobacter. Genes that are prevalent both in pathogenic and a-pathogenic Acinetobacter species were not considered ignoring that virulence factors may emerge by the modification of evolutionarily old and widespread proteins.
Here, we increased the resolution of comparative genomics analyses to also include lineage-specific changes in protein feature architectures. Using type IVa pili (T4aP) as an example, we show that three pilus components, among them the pilus tip adhesin ComC, vary in their Pfam domain annotation within the genus Acinetobacter. In most pathogenic Acinetobacter isolates, ComC displays a von Willebrand Factor type A domain harboring a finger-like protrusion, and we provide experimental evidence that this finger conveys virulence-related functions in A. baumannii. All three genes are part of an evolutionary cassette, which has been replaced at least twice during A. baumannii diversification. The resulting strain-specific differences in T4aP layout suggests differences in the way how individual strains interact with their host. Our study underpins the hypothesis that A. baumannii uses T4aP for host infection as it was shown previously for other pathogens. It also indicates that many more functional complexes may exist whose precise functions have been adjusted by modifying individual components on the domain level.
Author summary Type IVa pili (T4aP) are hair-like, extendable, and retractable appendages that many bacteria use for interacting with their environment. Several human pathogens have independently recruited these pili for processes related to host infection, but the modifications necessary to turn T4aP into virulence factors are largely unknown. Here, we studied if and how T4aP components have changed in the nosocomial pathogen A. baumannii compared to its largely a-pathogenic relatives in the Acinetobacter genus. Most A. baumannii isolates have T4aP with a pilus tip adhesin containing a protein domain variant not seen outside the pathogenic clade. This variant appears essential for bacterial motility and contributes to host cell adhesion and natural competence. However, some isolates have T4aP resembling those of largely a-pathogenic species in this genus. This indicates that the way these pili are used during infection processes differs between A. baumannii isolates probably as a consequence of niche adaptation. In a broader perspective, our findings highlight that many relevant genetic differences between pathogens and their a-pathogenic relatives emerge only on the domain- and sub-domain level. Thus, existing comparative genomics studies have likely uncovered only the tip of the iceberg of genetic determinants that contribute to A. baumannii virulence.
Iruegas R, Pfefferle K, Göttig S, Averhoff B, Ebersberger I (2023)
Feature architecture aware phylogenetic profiling indicates a functional diversification of type IVa pili in the nosocomial pathogen Acinetobacter baumannii. PLoS Genet 19(7): e1010646. https://doi.org/10.1371/journal.pgen.1010646
Copyright: © 2023 The authors.
Published by PLoS. Open access
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
They have the same problem with the malaria-causing Plasmodium parasites that Michael J Behe also used as an example (refuted again by Kenneth R. Miller) of irreducible complexity in the way it had evolved resistance to anti-malarial drugs.
Creationists need to decide whether these examples of 'irreducible complexity' that Behe keeps arguing falsely for are examples of the intervention of their favourite god, or of another creative entity over which their god apparently has no control, 'sin.
But perhaps these niceties are too subtle for the average creationist who only wants arguments that the Theory of Evolution is wrong because it doesn’t make them feel important enough.
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