Is Yersinia Pestis Evidence of Evolution
“Is Yersinia pestis evidence of evolution?”
🪫 “Is Yersinia pestis evidence of evolution?”
You’ve certainly heard of the plague — but have you ever wondered how it is contracted?
Simply put:
There is a bacterium called Yersinia pestis , which caused this disease that swept the world in the 14th century AD.
This bacterium originally lived in soil and caused nothing but indigestion —
but it “mutated” to develop into the horrific plague.
Evolutionists claim that this bacterium acquired this trait after having been nonexistent,
and then claimed that this is evidence of evolution.
As you know, our response to them comes from their own studies.
🧬 This bacterium acquired its ability through two methods:
- 1 – Acquiring the pYV plasmid and the inhalant :
Of course, this has nothing to do with evolution or the formation of new genes.
Rather, the plasmid was acquired from the surrounding environment through:
Transformation
Conjugation using sex pili
Or transduction using a bacterial virus
These genes are then meticulously integrated and genetically engineered.
In human pathogenic lineages, this was followed by a common pattern of acquisition of similar pathogenicity determinants, namely:
The virulence plasmid pYV
And the invasin ail
Then came the acquisition of further determinants within lineages, along with:
Functional gene loss
Reduced metabolic flexibility
🚫 2 – Gene losses of up to 317 genes ,
equivalent to 13% of the genome size ,
have conferred resistance to bacteria, and consequently:
Loss of functions
Even loss of some parts, such as the loss of some parts of the bacterial flagellum —
which has made them resistant.
In contrast, 149 other pseudogenes (doubling the previous estimate),
and 317 genes absent from Y. pestis were detected,
indicating that as many as 13% of Y. pseudotuberculosis genes no longer function in Y. pestis .
Extensive insertion sequence-mediated genome rearrangements
and reductive evolution through massive gene loss ,
resulting in elimination and modification of preexisting gene expression pathways,
appear to be more important than acquisition of genes
in the so-called “evolution” of Y. pestis .
🪫 These results provide a sobering example of how a highly virulent epidemic clone can suddenly emerge
from a less virulent, closely related progenitor.
🪫 Pathogenic yersiniae either repress flagella expression under host conditions (Yersinia enterocolitica and Yersinia pseudotuberculosis )
or have permanently lost this capability by mutation (Yersinia pestis ).
The block in flagella synthesis for the enteropathogenic Yersinia centers on fliA (sigmaF) repression .
This repression ensures the downstream repression of flagellin structural genes,
which can be cross-recognized and secreted by virulence type III secretion systems.
Y. pestis carries several flagellar mutations,
including a frameshift mutation in flhD , part of the flagellar master control operon.
Repression of flagellins in the host environment may be critical —
because they are potent inducers of innate immunity.
Artificial expression of flagellin in Y. enterocolitica completely attenuates virulence,
supporting the hypothesis that motility is a liability in the mammalian host.
🪫 “Pathogenic Yersinia either suppress flagellin gene expression under host conditions (Yersinia enterica and Yersinia pseudotuberculosis )
or permanently lose this ability due to mutation (Yersinia pestis ).
Inhibition of flagellin synthesis in pathogenic Yersinia is centered on the inactivation of fliA (sigmaF ).
This inhibition ensures the future inhibition of flagellin structural genes,
which can be recognized and secreted by type III virulence secretion systems.
Yersinia pestis carries several flagellin mutations, including a frameshift mutation in flhD — part of the master flagellin control operon.
Inhibition of flagellin in the host environment may be critical
because it is a potent inducer of innate immunity.
Artificial expression of flagellin in Yersinia enterica completely attenuates virulence,
supporting the hypothesis that motility is a barrier to mammalian hosts.”
📎 https://link.springer.com/chapter/10.1007/978-0-387-72124-8_27
🪫 It has been postulated that the genomes of Y. pestis have undergone functional reduction
as it made a transition from an orally and fecally spread pathogen causing gastroenteritis
to a vector-borne pathogen causing a fatal, invasive, septicemic disease,
where genes have been inactivated by various mechanisms such as:
Deletions/insertions
Frameshifts
Interruptions by insertion elements
Homologous or even nonhomologous recombination
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https://link.springer.com/chapter/10.1007/978-0-387-72124-8_27
A Rationale for Repression and/or Loss of Motility by Pathogenic Yersi
Pathogenic yersiniae either repress flagella expression under host conditions (Yersinia enterocolitica and Yersinia pseudotuberculosis) or have permanently lost this capability by mutation (Yersinia pestis). The block in flagella synthesis for the enteropathogenic…
- The team found that it was not only the acquisition of genes that has proven important to this family of bacteria,
but also the loss of genes and the streamlining of metabolic pathways seems to be an important trait for the pathogenic species.
The number of strain-specific lost functions was not equal among all strains.
In part, this can be explained by several large deletions that effectively delete many genes (functions) in a single event.
While strains 91001 and Antiqua had the greatest number of strain-specific function losses, with 69 and 41 , respectively,
it is interesting to note that CO92 was found to have the fewest compared to those of other strains.
Although strains Antiqua and 91001 share several gene inactivations (8 proteins ),
these are the result of independent mutations (homoplasy ),
while those lost in CO92 and Antiqua (12 proteins ),
as well as those lost in KIM and Nepal516 (16 proteins ),
share lineage-specific, inherited mutations (function losses ) that support the phylogenetic tree.
🪫 Of the 69 functional losses specific to 91001 :
24 are hypothetical proteins
7 are membrane proteins
7 are phage-related proteins
5 are regulatory proteins
3 are transporters
Some of these 91001-specific losses of function may be related to its human-avirulent phenotype.
Twenty-one of the 69 belong to a single IS285-mediated deletion event (YPO2108–YPO2134 ).
Ten of the 41 Antiqua-specific lost functions were the results of two deletion events.
Several inactivated or deleted genes were predicted to be directly or indirectly involved in interactions with the environment.
📌 For example:
YPO2367 , a glutathione S-transferase , is missing from the Antiqua genome.
The glutathione S-transferase family of enzymes routinely responds to oxidative stress or detoxification,
which can be encountered during entry into phagocytic cells .
Since bacteria usually have multiple glutathione S-transferases (CO92 has at least four based on annotation ),
losing one may not result in a distinct phenotype.
🪫 “The number of strain-specific loss of functions was not equal across all strains.”
This is partly due to multiple large deletions that effectively abolish several genes (functions) in a single event.
While strains 91001 and Antiqua had the highest number of strain-specific loss of functions —
at 69 and 41 , respectively —
it is interesting to note that CO92 had the fewest loss of functions compared to the other strains.
Although Antiqua and 91001 share several gene inactivations (8 proteins ),
these are the result of independent mutations (homoplasy ),
while the loss of functions in CO92 and Antiqua (12 proteins ),
as well as those in KIM and Nepal516 (16 proteins ),
share strain-specific inherited mutations (loss of functions) that support the phylogenetic tree.
Of the 69 loss of functions specific to 91001 :
24 are hypothetical proteins
7 are membrane proteins
7 are phage-associated proteins
5 are regulatory proteins
3 are transporter proteins
Some of these 91001-specific loss-of-function cases may be related to its human virulent phenotype.
Twenty-one of these 69 cases belonged to a single IS285-mediated deletion event (YPO2108–YPO2134 ).
Ten of the 41 Antiqua-specific loss-of-function cases were the result of two deletion events.
- Many of the inactivated or deleted genes are expected to have direct or indirect roles in interactions with the environment .
For example:
YPO2367 , a glutathione S-transferase , is missing from the Antiqua genome.
The glutathione S-transferase family routinely responds to oxidative stress or detoxification,
which may occur during phagocytic cell entry .
Since bacteria typically contain multiple glutathione S-transferases
(CO92 contains at least four based on the annotation ),
losing one may not result in a distinctive phenotype.
📎 https://www.pnas.org/doi/10.1073/pnas.1317161111
📎 https://www.sciencedaily.com/releases/2014/04/140421151933.htm
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https://www.sciencedaily.com/releases/2014/04/140421151933.htm
Plague in your family: Family tree of black death bacterium explored
The first view of the Black Death bacterium’s entire family tree shows some how family members evolve to become harmful. The researchers showed that Yersinia pestis and Yersinia enterocolitica, two major disease-causing species, independently acquired DNA that allowed them to become pathogenic.
