Photo by Nikolay Kolev (left) and Geoffrey Attardo (right)
This news item should please devotees of Creationism's putative intelligent [sic] designer, if for no other reason than that it involves a flagellum. Those who fell for Michael J Behe's opening ploy in his intelligent design hoax were fooled into believing that a flagellum is an irreducibly complex structure so must have been designed by an intelligent designer because it could not have evolved by Darwinian gradual evolution.
Of course, Behe ignored the fact that the component parts of the flagellar proton motor pre-existed the flagellum, in the Type II Secretion System, which was a development of the proton pump, so all that was needed was for them to be exapted for a different function, and to give the organism an advantage. It also ignores the fact that there are lots of different flagella found in nature, some with even fewer components than those of E. coli, which he had claimed was the minimum necessary for a functional flagellum. Clearly, if other flagella can work with less components, that of E. Coli is not irreducibly complex
And, unwittingly, Behe gave us the idea of a malevolent designer, because E. coli is much better at making us sick because it has a flagellum, than it would be without it. Given that Creationists believe their putative designer is omniscient, it must have been aware of that when it designed the flagellum.
Anyway, no matter how comprehensively the hoax is refuted, or how malevolent it makes their favourite god look, Creationists will ignore the science and stick with the refuted notion, so those are the people who should be thrilled by this discovery. It is the discovery that the trypanosomes carried by the tsetse fly, which causes sleeping sickness in humans and debilitating diseases in cattle and horses, has a flagellum specially designed to enable the tsetse fly to pass it on in its saliva when it takes a blood meal.
In 2010 it was estimated that, in Africa, diseases carried and transmitted by Tsetse flies kill an estimated 250,000 - 500,000 people and 3 million cattle a year, and costs an estimated 1-1.2 billion US$ a year (2010 figures).
Readers might remember how I wrote about the tsetse fly and how the trypanosomes it carries is responsible for the failure of Africans to progress much beyond subsistence farming in this blog and in my popular, book, Unintelligent Design: Refuting the Intelligent Design Hoax.
Creationists, Flying In The Face Of Reason
Malevolent Designer News - Sleeping Sickness
The Unintelligent Designer: Refuting the Intelligent Design Hoax
Now, scientists at the Ludwig-Maximilians University (LMU), München, Germany, together with colleagues from Paris, Rio de Janeiro, Antwerp, Aarhus, Bordeaux, and Kiel, have shown how the organism that causes sleeping sickness, Trypanosoma brucei, gets itself into the salivary glands of the tsetse fly ready to be injected into an animal host when the tsetse fly takes a blood meal. They found that a signalling apparatus at the flagellar tip of the protozoa controls the migration of trypanosomes, in the tsetse fly via the messenger known as cyclic adenosine monophosphate (cAMP). Ingenious, or what? The team have published their findings, open access, in Nature CommunicationsMalevolent Designer News - Sleeping Sickness
The Unintelligent Designer: Refuting the Intelligent Design Hoax
The LMU news release gives details of the research and the team's findings:
Technical details are give in the team's open access publication in Nature Communications:Tsetse flies are common across much of Africa. They feed on the blood of humans and other animals. In the process they can transmit trypanosomes, a protozoan parasite. Trypanosoma brucei causes sleeping sickness in humans. Pathogens infiltrate the host through the saliva of infected tsetse flies: from the blood, they reach the brain, leading to fatal symptoms if untreated.Tsetse Fly biting an animal host.
© picture alliance / © Bruce Coleman/Photoshot. | Kim Taylor
But how do trypanosomes get into the salivary glands of tsetse flies after their blood meal? Dr. Sabine Bachmaier and Professor Michael Boshart from the Genetics division at LMU’s Faculty of Biology, together with scientific colleagues, have found a surprising answer to this question. They show that a signaling apparatus at the flagellar tip of the protozoa controls the migration of trypanosomes in the tsetse fly via the messenger known as cyclic adenosine monophosphate (cAMP). The removal of a component of the enzyme complex that produces the cAMP signaling molecule was sufficient to prevent infection of the flies. Results of the study have now been published in Nature Communications.
Insights into the regulatory network
By way of background: Cattle and antelope are natural reservoirs of Trypanosoma brucei. During a blood meal, pathogens get into the gastrointestinal tract of tsetse flies. In order to survive and further propagate, trypanosomes need to adapt to their changing environment. They migrate back and forth between the bloodstream and the tissues of a mammalian host and between the digestive tract and the salivary glands of a tsetse fly, whereby they pass through a series of developmental stages.Our project is based on several international collaborations with research groups in Paris, Antwerp, and Rio de Janeiro. We’d long been interested in the question as to how parasites manage to orient themselves in the tsetse fly – and how this could be prevented in order to control transmission of the disease.
Our discovery that CARP3 is found primarily at the tip of the flagella of trypanosomes put us on the scent of a specialized signaling apparatus for the orientation of the parasites in the tsetse fly
[When we removed the CARP3 gene] trypanosomes were subsequently no longer able to efficiently colonize tsetse flies. In the salivary glands, we didn’t find a single cell of the parasites anymore.
Dr. Sabine Bachmaier, co-senior author
Faculty of Biology, Genetics,
Ludwig-Maximilians-University (LMU), Munich, Germany
Around ten years ago, the research group identified a new and trypanosome-specific component of the cAMP signaling pathway – the cyclic AMP response protein 3 (CARP3). When the researchers removed the CARP3 gene by means of genetic engineering, the composition of the enzymes (adenylate cyclases) that produce cAMP at the flagellar tip also changed.
From basic research to application: The objective of a long-term strategy could be to impair the interactions between CARP3 and adenylate cyclases. This could be done, for example, by means of a synthetic peptide that would be produced in the flies using the technique known as paratransgenesis. Without colonizing the salivary glands of tsetse flies, the trypanosomes would no longer be transmitted.
AbstractCreationists must be so impressed by the fanatical zeal and attention to detail in their beloved intelligent designer's determination to make us, and in this case, African's, sick, and increase their suffering!
Signaling from ciliary microdomains controls developmental processes in metazoans. Trypanosome transmission requires development and migration in the tsetse vector alimentary tract. Flagellar cAMP signaling has been linked to parasite social motility (SoMo) in vitro, yet uncovering control of directed migration in fly organs is challenging. Here we show that the composition of an adenylate cyclase (AC) complex in the flagellar tip microdomain is essential for tsetse salivary gland (SG) colonization and SoMo. Cyclic AMP response protein 3 (CARP3) binds and regulates multiple AC isoforms. CARP3 tip localization depends on the cytoskeletal protein FLAM8. Re-localization of CARP3 away from the tip microdomain is sufficient to abolish SoMo and fly SG colonization. Since intrinsic development is normal in carp3 and flam8 knock-out parasites, AC complex-mediated tip signaling specifically controls parasite migration and thereby transmission. Participation of several developmentally regulated receptor-type AC isoforms may indicate the complexity of the in vivo signals perceived.
Bachmaier, S., Giacomelli, G., Calvo-Alvarez, E. et al.
A multi-adenylate cyclase regulator at the flagellar tip controls African trypanosome transmission.
Nat Commun 13, 5445 (2022). DOI: 10.1038/s41467-022-33108-z
Copyright: © 2022 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
Imagine a real entity with that degree of hate-filled mendacity!
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