2023/07/22

Loss of information results in pathogenic bacteria

Bacteria prove genetic entropy. Evolution never happened.


Genome Reduction Is Associated with Bacterial Pathogenicity across Different Scales of Temporal and Ecological Divergence


Excerpts: "Emerging bacterial pathogens threaten global health and food security, and so it is important to ask whether these transitions to pathogenicity have any common features. We present a systematic study of the claim that pathogenicity is associated with genome reduction and gene loss. We compare broad-scale patterns across all bacteria, with detailed analyses of Streptococcus suis, an emerging zoonotic pathogen of pigs, which has undergone multiple transitions between disease and carriage forms. We find that pathogenicity is consistently associated with reduced genome size across three scales of divergence (between species within genera, and between and within genetic clusters of S. suis). Although genome reduction is also found in mutualist and commensal bacterial endosymbionts, genome reduction in pathogens cannot be solely attributed to the features of their ecology that they share with these species, that is, host restriction or intracellularity. Moreover, other typical correlates of genome reduction in endosymbionts (reduced metabolic capacity, reduced GC content, and the transient expansion of nonfunctional elements) are not consistently observed in pathogens. Together, our results indicate that genome reduction is a consistent correlate of pathogenicity in bacteria."

"The emergence of new bacterial pathogens is a major threat to human health and food security across the globe (Vouga and Greub 2016). Although every instance of pathogen emergence will be unique in some way, identifying common features could help us to understand, predict, and ultimately prevent these transitions to pathogenicity. One intriguing observation is that some of the most serious human pathogens have smaller genomes and fewer genes than their closest nonpathogenic or less pathogenic relatives (Pupo et al. 2000; Ochman and Moran 2001; Moran 2002; Stinear et al. 2008; Toft and Andersson 2010; Georgiades and Raoult 2011; Langridge et al. 2015; Weinert and Welch 2017)."

"The genomes of endosymbiotic bacteria often have lower GC contents than those of their free-living counterparts (Moran 2002). This could reflect metabolic adaptation to the host environment (Rocha and Danchin 2002; Dietel 2019), or a reduction in GC-biased gene conversion due to lower rates of recombination (Lassalle et al. 2015). But it is usually assumed to be a consequence of a reduced efficacy of selection, coupled with a bias towards GC-to-AT mutations (Hershberg and Petrov 2010; Hildebrand et al. 2010; McCutcheon and Moran 2012). Results shown in figure 3g–i, show that patterns of GC content in pathogens are more complicated than predicted. Between species, we did observe the predicted tendency for pathogens to be GC-poor."  

"By contrast, the core genome shows the reverse pattern, with isolates with smaller genomes being less GC rich (supplementary fig. S7d, Supplementary Material online). But this is only evident between genetic clusters, suggesting that accumulation of GC-to-AT mutations in the core genome is a slow process. The result is that the predicted association between pathogenicity and low GC is observed in S. suis, but only between clusters, and only in the core genome." (My add: Promoters and enhancers are located between genes. They are typically CpG islands and vulnerable to GC --> AT mutations.)

Other studies confirm the mutations are universally biased towards AT not only in bacteria but in all kind of organisms and viruses:

https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1001115
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7106825/

However, organisms have built in mechanisms by which they can sometimes compensate for the loss of gc content. These are for example transposons and gene duplications which are epigenetically driven mechanisms. Interesting observation is that rising temperatures cause GC --> AT mutations to occur more likely. 

Summary and conclusions:
  • Genome reduction is correlated with bacterial pathogenicity.
  • The most serious pathogenic bacteria have fewer genes than their closest, nonpathogenic relatives.
  • There is a predicted tendency for pathogens to be GC-poor.
  • Mutations are universally biased towards AT not only in bacteria but in all kind of organisms and viruses.
  • There is no DNA repair mechanism to reverse this phenomenon. In some cases the cell is able to compensate for the loss of information by using transposons or gene duplications. However, this doesn't change the universal tendency for GC --> AT mutations.
  • Evolution has no mechanism. Loss and corruption of information occurs rapidly and this observation refutes the theory of millions of years of evolution.

    p.s. I wrote about this already in 2018.

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