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| Black-legged or deer tick, Ixodes scapularis. Photo:Scott Bauer. This image was released by the Agricultural Research Service, the research agency of the US Department of Agriculture, with the ID k8002-3 (next)., Public Domain, Source: Wikipedia |
Here's a real treat for the followers of the intelligent [sic] designer and those who appreciate the length this malevolence is going to to make humans and other creatures sick.
The first is an account of how the Anaplasma phagocytophilum, tick-borne parasite that causes anaplasmosis, manages to live in the tick which the intelligent [sic] designer has chosen as the means of injecting it into its target hosts.
Scientists at the Department of Biological Sciences, Old Dominion University, Norfolk, Virginia, USA and Department of Entomology, Connecticut Agricultural Experiment Station, New Haven, Connecticut, USA have discovered that A. Phagocytophilum interferes with a tick gene. This gene normally produces a chemical which inhibits the production of OATP on which organisms such as A. Phagocytophilum depend. This results in more OATP and so more A. Phagocytophilum to infect a host with.
The team published their findings, open access in PLOS Genetics:
Abstract
The microRNAs (miRNAs) are important regulators of gene expression. In this study, we provide evidence for the first time to show that rickettsial pathogen Anaplasma phagocytophilum infection results in the down-regulation of tick microRNA-133 (miR-133), to induce Ixodes scapularis organic anion transporting polypeptide (isoatp4056) gene expression critical for this bacterial survival in the vector and for its transmission to the vertebrate host. Transfection studies with recombinant constructs containing transcriptional fusions confirmed binding of miR-133 to isoatp4056 mRNA. Treatment with miR-133 inhibitor resulted in increased bacterial burden and isoatp4056 expression in ticks and tick cells. In contrast, treatment with miR-133 mimic or pre-mir-133 resulted in dramatic reduction in isoatp4056 expression and bacterial burden in ticks and tick cells. Moreover, treatment of ticks with pre-mir-133 affected vector-mediated A. phagocytophilum infection of murine host. These results provide novel insights to understand impact of modulation of tick miRNAs on pathogen colonization in the vector and their transmission to infect the vertebrate host.
Author summary
This study provides novel evidence that shows that down-regulation of arthropod microRNA-133 leading to enhanced expression of organic anion transporting polypeptide is not only critical for rickettsial pathogen Anaplasma phagocytophilum survival in ticks but also for this bacterial transmission from vector to the vertebrate host. Understanding how pathogens manipulate vector-signaling repertoire for their benefit would lead to the development of strategies to block their transmission from vector to the vertebrate host.
Ellango Ramasamy, Vikas Taank, John F Anderson, Hameeda Sultana, Girish Neelakanta.
Repression of tick microRNA-133 induces organic anion transporting polypeptide expression critical for Anaplasma phagocytophilum survival in the vector and transmission to the vertebrate host.
PLOS Genetics, 2020; 16 (7): e1008856 DOI: 10.1371/journal.pgen.1008856
Copyright: © 2020 The authors.
Open Access
Reprinted under a Creative Commons Attribution 4.0 International Licence (CC BY 4.0)
Brilliant, or what?
No doubt intelligent [sic] design enthusiasts can explain the intelligence behind designing an organism to live off the OATP in the tick's cells, then in designing a mechanism for reducing this, presumably to inhibit the growth of the parasites, then redesigning the parasite to overcome the tick's defences. Superficially, it might seem to non-intelligent [sic] design advocates that this is a mark of gross stupidity and a needless increase in complexity simply to overcome a problem it created earlier to solve a problem it created in the first place - and all to make people sick!
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| Campylobacter jejuni |
Scientists reveal why tummy bugs are so good at swimming through your gut | Imperial News | Imperial College London
Hayley Dunning of Imperial College explains:
Campylobacter jejuni is responsible for millions of food poisoning cases every year, and a key step in its invasion of the body is swimming through the viscous (sticky) mucous layer of the guts. Researchers have observed that C. jejuni swims faster in viscous liquids than in less-viscous liquids, like water, but until now they didn’t know why.
Now, researchers from Imperial College London, Gakushuin University in Tokyo and the University of Texas Southwestern Medical Center have filmed C. jejuni in action to uncover the mystery. Their results are published today [June 2nd, 2020] in PLOS Pathogens.
Two opposing motors
C. jejuni uses its two opposing tails, called flagella, to help it move. It has a flagellum at each end of its body that spin around to propel itself through liquid. However, the opposing flagella have confused scientists.
Co-first author Dr Eli Cohen, from the Department of Life Sciences at Imperial, said: “It seemed very strange that the bacteria had a tail at both ends – it’s like having two opposing motors at either end of a ship. It was only when we watched the bacteria in action that we could see how the two tails work cleverly together to help the bacteria move through the body.”
C. jejuni cells bodies (red) and flagella (green)
The team created C. jejuni strains that have fluorescent flagella and used high-speed microscopy to see what happened as they swam around. They discovered that to move forward, the bacteria wrap their leading flagella around their helically shaped bodies, meaning both flagella were then pointing in the same direction and providing unified thrust.
To change direction, they changed which flagella were wrapped around their body, enabling quick 180 degree turns and potential escape from confined spaces.
Sticky situations
They also found that the process of wrapping the flagella was easier when swimming through viscous liquids; the stickiness helping push the leading flagella back around the body. In less-viscous liquids neither flagella were able to wrap around the body.
Lead researcher Dr Morgan Beeby, from the Department of Life Sciences at Imperial, said: “Our study kills two birds with one stone: in setting out to understand how C. jejuni moves, we resolved the apparent paradoxes of how it swims in one direction with opposing flagella and how it swims faster in more viscous liquids.
The team's paper can be read, open access in PLOS Pathogens:
Abstract
Campylobacter jejuni rotates a flagellum at each pole to swim through the viscous mucosa of its hosts’ gastrointestinal tracts. Despite their importance for host colonization, however, how C. jejuni coordinates rotation of these two opposing flagella is unclear. As well as their polar placement, C. jejuni’s flagella deviate from the norm of Enterobacteriaceae in other ways: their flagellar motors produce much higher torque and their flagellar filament is made of two different zones of two different flagellins. To understand how C. jejuni’s opposed motors coordinate, and what contribution these factors play in C. jejuni motility, we developed strains with flagella that could be fluorescently labeled, and observed them by high-speed video microscopy. We found that C. jejuni coordinates its dual flagella by wrapping the leading filament around the cell body during swimming in high-viscosity media and that its differentiated flagellar filament and helical body have evolved to facilitate this wrapped-mode swimming.
Author summary
Campylobacter jejuni is a leading cause of gastroenteritis worldwide. This species uses its helical body and opposing flagella to drill its way through the viscous mucosa of host organisms’ gastrointestinal tracts. In this work, we show that C. jejuni coordinates its two opposing flagella by wrapping the leading flagellum around the cell body when swimming in viscous environments. We also provide evidence that the helical cell body of C. jejuni and its composite flagellar filament are important for wrapping and unwrapping of the flagellar filament during reversals of swimming direction.
Cohen EJ, Nakane D, Kabata Y, Hendrixson DR, Nishizaka T, Beeby M (2020)
Campylobacter jejuni motility integrates specialized cell shape, flagellar filament, and motor, to coordinate action of its opposed flagella. PLoS Pathog 16(7): e1008620. https://doi.org/10.1371/journal.ppat.1008620
Open Access
Reprinted under a Creative Commons Attribution 4.0 International License (CC BY 4.0)
So there we have another ingenious solution to a problem of the intelligent [sic] designer's own making. It had created an organism for causing gastroenteritis in humans and then had to devise a complicated mechanism so it could do its work in the environment it had been designed ro work in.
The delicious irony of this is that it had to substantially redesign that structure so beloved of intelligent [sic] design enthusiasts, the bacterial flagellum - the one it designed for E. coli not being up to the task apparently.
I wonder if MIchael J. Behe ever dreamt that his intelligent design hoax would be so easy to mock and would make his acolytes look like credulous simpletons when he invented it.
I love these posts...it amazes me how willfully ignorant and illogical the masses can be. Lately I have been wondering if our species is beginning to de-evolve. I have thought about does evolution reverse and also the third ( I believe) law of thermodynamics, where everything eventually degrades into chaos or something like that. The human race seems to be in chaos now.
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