F Rosa Rubicondior: Unintelligent Design
Showing posts with label Unintelligent Design. Show all posts
Showing posts with label Unintelligent Design. Show all posts

Tuesday 12 March 2024

Unintelligent Malevolence - Pathogens 'Designed' to Beat Medical Science In Two Different Ways


Acinetobacter baumannii seen under a scanning electron-microscope

Escherichia coli
What makes a pathogen antibiotic-resistant? | Sanford Burnham Prebys

One of todays examples of the stupidity of creationism is something of a novelty. Usually, by applying the central tenets of creationism, any putative designer of living things like parasites either appears malevolent (and sometime it has to be said, malevolent at a near genius level in the ways it finds to make us and other animals sick) or it looks incompetent in that its 'solutions' are often to problems of its own making and more often than not to solutions it designed for one side of an arms race which it now trets as problems for the other side.

But today's example can only be described as an example of incompetent malevolennce, as creationism's putative designer, faced with the same 'problem' of medical science developing antibiotics effective against two different species of pathogen, set about designign two completely different 'solutions' to this problem. - Talk about re-inventing the wheel!

The pathogens are: Escherichia coli and Acinetobacter baumannii.

Creationists will probably be familiar with Escherichia coli (E. coli) because they believe their guru, Michael J Behe, 'proved' their god exists by claiming (falsely) that E. coli's flagellum must have been intelligently designed because he didn't know it evolved out of a pre-exiting structure and couldn't think how else it could have evolved. But then such is the standard of creationist apologetics!

What Behe had unwitting done was destroy the traditional excuse creationists use to explain pathogens like E. coli by blaming them on another 'designer' called 'Sin' which somehow creates living organisms although the creationit designer god is the only entitiy capable of designing livign things, so any example of 'intelligent design, real or imaginary, if 'proof' of this designer god's existance.

So, what creationists are now left with is an E.coli with a flegellum designed by their god to make it better at making us sick, and now resitant to antibiotics to help it win against medical science trying to prevent it makign us sick!

But what creationists are less likely to be familiar with is the pathogen, Acinetobacter baumannii, so here is a little background:

Monday 11 March 2024

Unintelligent Design - RuBisCO Is Slowly Evolving - And Becoming Even More Embarrassing For Any Creationist Who Understands It


The world’s most prolific CO2-fixing enzyme is slowly getting better | University of Oxford

The world’s worst enzyme, ribulose-1,5-bisphosphate carboxylase/oxygenase, or RuBisCo as it is known, has featured in these blog posts several times and it described in my book, The Unintelligent Designer: Refuting the Intelligent Design Hoax as an example of the lack of intelligence in biological systems, and, as such, why it would be a major embarrassment to creationists - if they understood it.

Briefly, RuBisCo is one of the most ancient enzymes known and became an essential component of photosynthesis early on in the history of life on Earth when the first cyanobacteria evolved the ability to use the energy from sunlight to fix the carbon in atmospheric carbon dioxide (CO2) to build the sugar glucose. Eventually, these photosynthesising cyanobacteria became incorporated into plant cells as the chloroplasts to produce the green plants at the base of most food chains. Because it is so inefficient, it quickly became probably the most abundant enzyme on Earth, making up with quantity what it lacked in quality.

But, evolution, unlike good intelligent design, is a one-way, utilitarian process in which whatever works better than preceded it will be retained and will provide the next basis for further evolution, because evolution has no mechanism to scrap a bad design and start again as any backward step will inevitably be worse, so will be quickly eliminated.
Tell me all about RuBisCo and why it's so inefficient. RuBisCo, or ribulose-1,5-bisphosphate carboxylase/oxygenase, is an enzyme crucial for the process of carbon fixation in plants, algae, and some bacteria. It catalyzes the first major step of the Calvin cycle, which is the primary pathway for carbon dioxide fixation in photosynthesis. Despite its importance, RuBisCo is often considered inefficient for several reasons:

Sunday 10 March 2024

Unintelligent Design - How Epigenetic Settings Are Passed To Daughter Cells - Even William Heath Robinson Would Be Impressed


Cracking Epigenetic Inheritance: HKU Biologists Discovered the Secrets of How Gene Traits are Passed on - Press Releases - Media - HKU

It all started when single-celled organisms started to form colonies of like-minded individuals. The easiest way to do it was for the two daughter cells of a dividing cell to stick together instead of going their own way. They in turn would have had more daughter cells until they formed large clump of cells, but, unless the cells began to perform distinct functions, there was no advantage to forming clumps like that instead of each cell going its own way and fending for itself. Fortunately, there were no large predators around, otherwise a clump of cells would have made a tasty snack and the whole idea would have been abandoned as too risky by half, and we would be stuck now with a world of single-celled organisms and nothing else.

However, with the trial and error which characterises biological development, some of the cells in the clump began to perform specialist functions. For example, as the clump got larger, specialist cells would have been needed to exchange gasses with the environment or the cells at the centre would have been deprived of oxygen and their waste in the form of carbon dioxide would have accumulated because diffusing across a large mass of cells would be too slow to keep up with production and the supply of oxygen would be too slow to keep up with the demand. The same thing applied to getting nutrients into the center of the clump.

So, the clumps which had specialist cells fared better in the competition for resources than those which were just undifferentiated clumps. In fact, the clumps with specialised cells would probably have eaten the undifferentiated clumps and become predators. And with predators there was pressure for increased specialisation for movement, ingestion and excretion, for more efficient respiration and for reproduction. And predation also produced pressure for more motility, for senses like sight and smell and maybe hearing and as the organisms became more complex so they needed nervous systems to coordinate their activities and process and respond to the stimuli their senses were receiving from their environment and some would have evolved defensive armour such as scales and spikes and hard shells and internal structures like cartilage and bone to give their bodies shape and form and to make their swimming apparatus stiffer and more powerful.

But what they never managed to do was find a different way to produce all the different specialist cells by a different method to that used by their single-celled ancestors, so every cell in their body had the full genome whether they needed it or not, and more often than not, they didn't need most of it. A bone cell doesn't need to do what a nerve cell does, and a nerve cell doesn't need to do what a muscle cell does, and neither muscle nor nerve cells need to make bone, and what else needs to make elbow skin other than an elbow skin cell, except perhaps a scrotum skin cell? Yet they all have the genes for doing everything any one cell needs to do.

So, cue creationism's intelligent [sic] designer who has been designing and modifying all these different clumps of specialised cells but who, for some reason, seems incapable of recognising that its designs are heading for disaster unless it can think up a way to make sure each specialised cell has only the genes it needs. For reasons which no creationist apologist has ever managed to explain, their putative designer always behaves as though it can't undo a bad design and start again but is compelled to try to make the best of what it has muddled through with so far. In every way, creationism’s 'intelligent [sic] designer' behaves just like a mindless process operating without a plan, handicapped by acute amnesia, and constantly surprising itself with a new problem it designed just yesterday.

Just like the eccentric British designer and cartoonist, William Heath Robinson, no solution to a problem can be too complex even if it creates a new problem for which another overly complex solution has to be found. Unlikely objects, designed for a completely different purpose, will be pressed into service; a stepladder will be balanced precariously on top of a piano and an umbrella will be used to push a button when prodded by a sink plunger swinging on a length of knotted string. A labour-saving device for peeling potatoes will take half a dozen, intense and serious-looking men to operate it and peeling the potatoes will take considerably longer than had each man been given a potato peeler and left to get on with it. Eggs will be fried in a frying pan held over a candle lit by a match rubbed against a matchbox which swings into action when released by a lever when the scuttle-full of coal, or the boulder suspended on knotted string, lands on it.
Every hot-air ballon will have had several leaks mended with patches in a different fabric as will every set of bellows used to blow out the candle at the right time or make the fire burn up when needed to make the hot air balloon rise, which will be held down by a coal-scuttle full of coal until a man with nothing else to do, cuts the string with a pair of scissors when prodded in the back by an umbrella operated by a wheel with broken spokes joined together with sticks tied on with more string or held together with bent nails.

And the whole 'irreducibly complex', 'intelligently designed' machine would fail if just one component was taken away or a piece of knotted string broke.
So, what did creationism's intelligent designer produce to solve the problem of too many genes for the specialised cells? It produced the overly complex solution of epigenetics of course! There was no going back and starting again for our intrepid, muddle through, mend and make do, near-enough-is-good-enough utilitarian designer. Going back and starting again would have been far too simple.

So complex is this system, that a team of researchers has only just worked out how cells pass on their epigenetic settings to their daughter cells.

Their findings are the subject of a paper in Nature and a news release from the University of Hong Kong:

Figure 2.The cryo-EM structure of the yeast replisome in complex with FACT and parental histones (A) and its atomic model (B).
Modified from Li et al, Nature (2004)
Figure 2. The cryo-EM structure of the yeast replisome in complex with FACT and parental histones (A) and its atomic model (B).
Modified from Li et al, Nature (2004)
A research team led by Professor Yuanliang ZHAI at the School of Biological Sciences, The University of Hong Kong (HKU) collaborating with Professor Ning GAO and Professor Qing LI from Peking University (PKU), as well as Professor Bik-Kwoon TYE from Cornell University, has recently made a significant breakthrough in understanding how the DNA copying machine helps pass on epigenetic information to maintain gene traits at each cell division. Understanding how this coupled mechanism could lead to new treatments for cancer and other epigenetic diseases by targeting specific changes in gene activity. Their findings have recently been published in Nature.

Background of the Research

Our bodies are composed of many differentiated cell types. Genetic information is stored within our DNA which serves as a blueprint guiding the functions and development of our cells. However, not all parts of our DNA are active at all times. In fact, every cell type in our body contains the same DNA, but only specific portions are active, leading to distinct cellular functions. For example, identical twins share nearly identical genetic material but exhibit variations in physical characteristics, behaviours and disease susceptibility due to the influence of epigenetics. Epigenetics functions as a set of molecular switches that can turn genes on or off without altering the DNA sequence. These switches are influenced by various environmental factors, such as nutrition, stress, lifestyle, and environmental exposures.

In our cells, DNA is organised into chromatin. The nucleosome forms a fundamental repeating unit of chromatin. Each nucleosome consists of approximately 147 base pairs of DNA wrapped around a histone octamer which is composed of two H2A-H2B dimers and one H3-H4 tetramer. During DNA replication, parental nucleosomes carrying the epigenetic tags, also known as histone modifications, are dismantled and recycled, ensuring the accurate transfer of epigenetic information to new cells during cell division. Errors in this process can alter the epigenetic landscape, gene expression and cell identity, with potential implications for cancer and ageing. Despite extensive research, the molecular mechanism by which epigenetic information is passed down through the DNA copying machine, called the replisome, remains unclear. This knowledge gap is primarily due to the absence of detailed structures that capture the replisome in action when transferring parental histones with epigenetic tags. Studying the process is challenging because of the fast-paced nature of chromatin replication, as it involves rapid disruption and restoration of nucleosomes to keep up with the swift DNA synthesis.

In previous studies, the research team made significant progress in understanding the DNA copying mechanism, including determining the structures of various replication complexes. These findings laid a solid foundation for the current research on the dynamic process of chromatin duplication.

Summary of Research Findings

This time, the team achieved another breakthrough by successfully capturing a key snapshot of parental histone transfer at the replication fork. They purified endogenous replisome complexes from early-S-phase yeast cells on a large scale and utilised cryo-electron microscopy (cryo-EM) for visualisation.

They found that a chaperone complex FACT (consisting of Spt16 and Pob3) interacts with parental histones at the front of the replisome during the replication process. Notably, they observed that Spt16, a component of FACT, captures the histones that have been completely stripped off the duplex DNA from the parental nucleosome. The evicted histones are preserved as a hexamer, with one H2A-H2B dimer missing. Another protein that involved in DNA replication, Mcm2, takes the place of the missing H2A-H2B dimer on the vacant site of the parental histones, placing the FACT-histone complex onto the front bumper of the replisome engine, called Tof1. This strategic positioning of histone hexamer on Tof1 by Mcm2 facilitates the subsequent transfer of parental histones to the newly synthesised DNA strands. These findings provide crucial insights into the mechanism that regulates parental histone recycling by the replisome to ensure the faithful propagation of epigenetic information at each cell division.

This study, led by Professor Zhai, involved a collaborative effort that spanned nearly eight years, starting at HKUST and concluding at HKU. He expressed his excitement about the findings, ‘It only took us less than four months from submission to Nature magazine to the acceptance of our manuscript. The results are incredibly beautiful. Our cryo-EM structures offer the first visual glimpse into how the DNA copying machine and FACT collaborate to transfer parental histone at the replication fork during DNA replication. This knowledge is crucial for elucidating how epigenetic information is faithfully maintained and passed on to subsequent generations. But, there is still much to learn. As we venture into uncharted territory, each new development in this field will represent a big step forward for the study of epigenetic inheritance.’

The implications of this research extend beyond understanding epigenetic inheritance. Scientists can now explore gene expression regulation, development, and disease with greater depth. Moreover, this breakthrough opens up possibilities for targeted therapeutic interventions and innovative strategies to modulate epigenetic modifications for cancer treatment. As the scientific community delves deeper into the world of epigenetics, this study represents a major step towards unravelling the complexities of replication-coupled histone recycling.

About the Research Team

Apart from Professor Yuanliang Zhai’s lab, the research team also includes Professor Xiang David Li from Department of Chemistry of HKU, Professor Yang Liu and Professor Keda Zhou from School of Biomedical Sciences of HKU, Professor Shangyu Dang from Division of Life Science of HKUST, and others. Learn more about Professor Yuanliang Zhai’s work and his research team: https://www.scifac.hku.hk/people/zhai-yuanliang or https://zhai95.wixsite.com/mysite-1

Co-authors include Mr Yuan Gao, Mr Jian Li, Dr Zhichun Xu from School of Biological Sciences (SBS) of HKU; Dr Ningning Li, Ms Yujie Zhang, Dr Jianxun Feng from School of Life Sciences of PKU, Dr Daqi Yu and Dr Jianwei Lin from Department of Chemistry of HKU, and Dr Yingyi ZHANG from Biological Cryo- EM Center of HKUST.

The journal paper can be accessed here: https://www.nature.com/articles/s41586-024-07152-2

Abstract

In eukaryotes, DNA compacts into chromatin through nucleosomes1,2. Replication of the eukaryotic genome must be coupled to the transmission of the epigenome encoded in the chromatin3,4. Here we report cryo-electron microscopy structures of yeast (Saccharomyces cerevisiae) replisomes associated with the FACT (facilitates chromatin transactions) complex (comprising Spt16 and Pob3) and an evicted histone hexamer. In these structures, FACT is positioned at the front end of the replisome by engaging with the parental DNA duplex to capture the histones through the middle domain and the acidic carboxyl-terminal domain of Spt16. The H2A–H2B dimer chaperoned by the carboxyl-terminal domain of Spt16 is stably tethered to the H3–H4 tetramer, while the vacant H2A–H2B site is occupied by the histone-binding domain of Mcm2. The Mcm2 histone-binding domain wraps around the DNA-binding surface of one H3–H4 dimer and extends across the tetramerization interface of the H3–H4 tetramer to the binding site of Spt16 middle domain before becoming disordered. This arrangement leaves the remaining DNA-binding surface of the other H3–H4 dimer exposed to additional interactions for further processing. The Mcm2 histone-binding domain and its downstream linker region are nested on top of Tof1, relocating the parental histones to the replisome front for transfer to the newly synthesized lagging-strand DNA. Our findings offer crucial structural insights into the mechanism of replication-coupled histone recycling for maintaining epigenetic inheritance.

This Heath-Robinson solution to a problem which no intelligent designer would design in the first place, is repeated in every one of your 17 trillion cells and in every cell of every multicellular organism on the planet. A hugely wasteful and error-prone, needlessly complex system of which any intelligent designer would be ashamed, but which creationist frauds fool their ignorant dupes into believing is evidence of intelligence. In reality of course, it's evidence of exactly the opposite.

It's not even humorous and entertaining like William Heath-Robinson's ridiculously complicated, irreducibly complex, machines.

Saturday 2 March 2024

Unintelligent Design - The Heath-Robinson Workaround For A Design Fault In The Immune System


The “switch” that keeps the immune system from attacking the body - EPFL

A Machine for Testing Golf Drivers - William Heath-Robinson
A characteristic of designs by creationism's putative intelligent designer, is the needless complexity which often arises because earlier solutions were suboptimal and either didn't work very well or tended to cause problems that needed to be mitigated with another layer of (often suboptimal) complexity.

This is also a characteristic of systems 'designed' by a mindless natural process with no power or mechanism for scrapping a suboptimal design and starting again and no ability to predict the future and design for problems which will arise later.

In fact, what creationists think is evidence of a supreme intelligence, more often seems to resemble the designs of the British cartoonist and eccentric designer, William Heath-Robinson, who was famous for his machines designed to solve every-day problem, which were invariably far more complex than they need have been, and which incorporated everyday objects such as umbrellas, full coal-scuttles for counter-weights, lengths of knotted string and stepladders balanced on upright pianos to give them enough height. Take away any of these unlikely components and the whole machine would fail, in an almost perfect metaphor for how evolution can exapt pre-exiting structures from other processes and structures for novel functions, to give the appearance of irreducible complexity.

And yet they work, or at least look as though they would if anyone ever made one.

An example of a Heath-Robinson machine in mammalian 'design' was revealed by a scientists working at the Swiss École polytechnique fédérale de Lausanne (EPFL), who have discovered how the body prevents the immune system from attacking itself.

But, as the very many auto-immune diseases show, this system is far from perfect and frequently fails, sometime with serious, even fatal, consequences.

But the whole immune system is only needed because something designed pathogens such as bacteria, viruses and other parasites, apparently to attack us and make us sick in the first place. Parasites are a source of conflict for creationists who have to believe both that the putative designer god is the only entity capable of designing living things, and that something else created parasites because their god wouldn't do such a thing, and both that their god is omnipotent, but powerless against that other designer.

So, what is this mechanism the EPFL researchers have discovered?

Their findings are the subject of an open access paper in Nature and is explained in an EPFL news release:

Friday 1 March 2024

Malevolent Designer News - How Creationism's Divine Malevolence Is Adapting The Avian Flu Virus to Kill Marine Mammals


Avian Influenza Virus Is Adapting to Spread to Marine Mammals | UC Davis

Elephant seals lie dead on a beach in Argentina following an outbreak of avian influenza in the region.
Photo: Maxi Jonas.
As an example of creationist double-think and intellectual bankruptcy, their attitude toward parasites like viruses is a classic:
  • "Only God is capable of designing organisms, so "Look at the trees!" and "What about irreducible complexity?"
  • "Something else created parasites like bacteria, worms and viruses, because God wouldn't do something like that!"

Simultaneously committing blasphemy and refuting their own argument from teleology!

I wonder then how that rarest of animals, the intellectually honest creationist copes with the news that the creator of the avian flu virus, H5N1, is in the process of adapting it to kill marine mammals such as elephant seals, just as it adapted the SARS-CoV-2 virus from a bat virus to one that could kill humans and cause economic collapse.

Evidence that it is doing so, if you believe viruses are created and don't evolve naturally, which dogma forbids a creationist from believing, comes in the form of a study by scientists from University of California, Davis, and the National Institute of Agricultural Technology (INTA) in Argentina. The study, the first genomic characterization of H5N1 in marine wildlife on the Atlantic shore of South America, is published in the journal Emerging Infectious Diseases and is described in a UC Davis news release:

Thursday 29 February 2024

Malevolent Designer News - Creationism's Divine Malevolence Is Still Victimising Frogs


Foothill yellow-legged frog, Rana boylii

Photo: Rebecca Fabbri/USFWS
Scientists assemble a richer picture of the plight and resilience of the foothill yellow-legged frog | The Current

Almost unnoticed by the general public and noticed only by biologists and wildlife conservationists, is a pandemic far more deadly than the Covid-19 pandemic, or even the Medieval Black Death.

It kills a very high percentage of its victims, has already exterminated whole populations of frogs and other amphibians, and has contributed significantly to the global mass extinction currently underway.

It is, of course, the chytrid fungus Batrachochytrium dendrobatidis, which, along with a closely-related fungus, B. salamandrivorans, causes the fatal disease, chytridiomycosis, in frogs and other amphibians.

As an example of the work of creationism's divine malevolence, it takes some beating for its sheer malevolent nastiness. It infects the skin of these amphibians, through which they breath, and causes it to thicken and fail as a respiratory organ, leading to suffocation, multiple organ failure and death. Here is how I described it in my illustrated book, The Malevolent Designer: Why Nature's God is not Good:
Exterminating Frogs with a Fungus.

Most of the examples I’ve talked about so far have been organisms and viruses that affect humans, but we are far from being the only species that Creationism’s putative intelligent designer seems to have taken an intense dislike to. For example, the world’s frogs and other amphibians are currently being decimated by chytridiomycosis, caused by a couple of related Chytrid fungi, Batrachochytrium dendrobatidis and B. salamandrivorans. It has been estimated that over 500 different species have been severely reduced in number by this fungal plague, with over 90 extinctions.

These fungi seem to have originated in an area of Southeast Asia by modification of a common, harmless, soil fungus. In that part of the world, the local population of amphibians seems to be resistant to the pathogenic forms of the fungi, suggesting that these fungi frequently become pathogenic and the local population have built up resistance to it.

According to research carried out by a team from the Fenner School of Environment and Society, Australian National University, ACT, Australia, it was resistance in the local population which probably kept the disease from spreading more widely, until human agency intervened to change the environment. They have related the increased trade in amphibian species to the spread of the fungi all over the world where they found species with no evolved resistance (42).

Figure 5 Frog Victims of Chytrid Fungus

Illustration: Catherine Webber-Hounslow
Recently, another team found that one of the factors that could have made these fungi so successful is that the frog’s immune response seems to have worked against it. Researchers from the University of Central Florida and the Smithsonian Conservation Biology Institute (SCBI) found that, in the frog Rana yavapaiensis, a species known to vary in its ability to survive attack by these fungi, those which showed an elevated immune response had a worse outcome that those with a lower response (43). Somehow, the frog’s ‘designed’ immune system was working against it and the fungi had been ‘designed’ to exploit this.

ID advocates would have us believe that, for reasons unknown, their putative intelligent designer has deliberately redesigned a soil fungus so it can overcome the immune system it designed to protect frogs from infections, and so exterminate over 90 species of amphibians that it designed earlier and severely endanger some 500 species in what has been described as the biggest single loss of biodiversity, albeit, aided and abetted by humans in this endeavour. Creationism’s intelligent designer must really hate the frogs it designed. Maybe a private definition of the word ‘intelligent’ is being employed here.
Now a team of researchers from multiple American wildlife and conservation agencies have looked in detail at the spread of this fungus in one particular frog which has declined so rapidly it is now an endangered species - the foothill yellow-legged frog, Rana boylii. This small frog's range once extended from Oregon to Baja California.

They have shown that human agency is implicated in the spread of this fungus by not only spreading it around the world in trade, as the earlier Australian study found (42), but with regard to the foothill yellow-legged frog specifically, by global warming, climate change and habitat destruction as more land is converted to agriculture. They have published their work, open access, in Royal Society Open Science. It is also explained in a University of California Santa Barbara, news release:

Up to only a few inches in length, with a lemon-hued belly, the foothill yellow-legged frog may seem unassuming. But its range once stretched from central Oregon to Baja California. In 2023, it was listed under the federal Endangered Species Act. Its rapidly decreasing range is due in part to a fungal pathogen called Batrachochytrium dendrobatidis, or Bd, that has devastated amphibians around the world.

A team of researchers, including UC Santa Barbara’s Andrea Adams, has conducted the most comprehensive study to date of disease dynamics in foothill yellow-legged frogs. The team’s data — sourced from both wild frogs and specimens in museum collections — enabled them to track patterns of infection across a large geographic range. In a study published in Royal Society Open Science, the researchers reveal that drought, rising temperatures and the increasing conversion of land for agriculture appear to be the largest factors driving Bd infection in this species.

The researchers aimed to assemble as much data as they could, both in space and time. They surveyed in the creeks and rivers of California and Oregon, where they swabbed wild yellow-legged frogs for the presence of Bd. It also led them into fluorescent-lit museum collections to sample specimens from as far back as the 1890s.

The team leveraged a large network of people and institutions to amass this wealth of samples.

Many foothill yellow-legged frog field researchers had data that they weren’t actively analyzing, and so we were able to bring all of this data together and get it into a usable format that we could use to paint a much bigger picture of what is, and was, going on with Bd in this species.

Andrea J. Adams, co-author.
Earth Research Institute
University of California, Santa Barbara, CA, USA.
The researchers swabbed each frog’s skin to determine if the animal was infected. To test for Bd, they used a PCR test, similar to some tests for COVID. By searching for Bd DNA from thousands of samples, the researchers were able to identify infection rates and severity. Co-lead author Ryan Peek ran this information through statistical models, which accounted for climatic, geographic, biologic and land use variables. This enabled the team to track disease patterns across a large geographic range over roughly 120 years.

The team discovered that disease patterns of Bd aligned with historical frog declines. The pathogen began to spread in the 1940s from the southern coast of California, moving northward and eventually affecting nearly the entire region. The biggest factors driving infection seem to be drought, increasing temperatures and the use of ever more land for agriculture.

Bd is a fungus that is spread through spores in the water, but that spread may occur differently in foothill yellow-legged frogs in different regions and climates, the researchers found. In some places, drought increased infection, while in others, it did not, possibly because of the presence or absence of other species that can carry Bd and share the same water, such as American bullfrogs, a species introduced from eastern North America.

If you combine the fact that there are bullfrogs building up the number of spores that these frogs are exposed to, and then they’re all kind of stuck in these small pools together, that explains why drought matters. They are suddenly getting hit with a really large number of spores and getting sick and dying.

These findings open more questions about what was stopping transmission and what allowed it to happen later.

Dr. Anat M. Belasen, co-first author
Department of Integrative Biology
University of Texas at Austin, Austin, TX, USA
And Department of Ecology and Evolutionary Biology,
Cornell University, Ithaca, NY, USA.
What’s more, foothill yellow-legged frogs live exclusively in streams and rivers, not ponds and lakes. So the species is already stressed when these waterways shrink into isolated pools.

The progression of Bd in the foothill yellow-legged frog also differed from its course in other western amphibians. In many other species, the disease radiated from urban centers, rather than this clear south-to-north trend. What’s more, the disease showed up later in the foothill yellow-legged frog than in other species in its range.

Frogs switch from herbivores as tadpoles to carnivores as adults, which means they connect different nutrient cycles together in the food web. Their position at the center of the food chain also influences the ecosystem.

When you remove frogs from an ecosystem, what you get is less control of insects, things that the frogs would eat. There is also less food for things that eat the frogs, like snakes, birds and small mammals. It really throws things off and makes the ecosystem less stable and less functional.

“There are areas that have wet soils that would be alongside suitable habitat. In areas where more of those lands have been converted to agriculture, we see a higher risk of frogs being infected with the fungus.

Dr. Anat M. Belasen.
Co-author Jamie Bettaso swabs a wild foothill yellow-legged frog to test for fungal infection.

Photo Credit: Jamie Bettaso
The conversion of land for agriculture was another major factor influencing the spread of Bd. for these frogs.

In addition to disease hotspots, the team also identified a number of cold spots — areas where the pathogen is present but less influential. The existence of so many cold spots in different areas is a good sign, as it may mean that many areas have conditions suitable for keeping disease rates low, even as climate change increases temperatures and patterns of drought.

The authors are curious what might explain this clustering, especially when cold spots appear in unexpected locations: for example, places with similar habitat, land-use and climatic impacts as hotspots. It suggests there may be some genetic basis for the differences, whether on the pathogen side or the host side. Adams is currently researching the feasibility of reintroducing foothill yellow-legged frogs to Southern California.

The results of this paper shed a lot of light on the dynamics of where Bd occurs, what drives its spread and how the pathogen and frog may interact in the future.

We took a big snapshot of this species’ disease relationship through time. Earlier studies provided the researchers with glimpses into disease patterns in smaller geographic regions, “but now we have a much larger dataset that further confirms many of these patterns, and expands on them.

Andrea J. Adams.
More detail is given in the team's open access paper in Royal Society Open Science:
Abstract

Species with extensive geographical ranges pose special challenges to assessing drivers of wildlife disease, necessitating collaborative and large-scale analyses. The imperilled foothill yellow-legged frog (Rana boylii) inhabits a wide geographical range and variable conditions in rivers of California and Oregon (USA), and is considered threatened by the pathogen Batrachochytrium dendrobatidis (Bd). To assess drivers of Bd infections over time and space, we compiled over 2000 datapoints from R. boylii museum specimens (collected 1897–2005) and field samples (2005–2021) spanning 9° of latitude. We observed a south-to-north spread of Bd detections beginning in the 1940s and increase in prevalence from the 1940s to 1970s, coinciding with extirpation from southern latitudes. We detected eight high-prevalence geographical clusters through time that span the species' geographical range. Field-sampled male R. boylii exhibited the highest prevalence, and juveniles sampled in autumn exhibited the highest loads. Bd infection risk was highest in lower elevation rain-dominated watersheds, and with cool temperatures and low stream-flow conditions at the end of the dry season. Through a holistic assessment of relationships between infection risk, geographical context and time, we identify the locations and time periods where Bd mitigation and monitoring will be critical for conservation of this imperilled species.

1. Introduction

Threatened species with large geographical ranges often require unique, regional conservation strategies to combat stressors such as infectious disease. Pathogen surveys and reporting have become standard for North American wildlife diseases [1,2]; however, relative risk across a landscape and among populations within species remains difficult to anticipate, especially when data are collected by separate research groups [3]. Central reporting databases [4], synthetic analyses and retrospective surveys can help assess disease threats and identify high-risk populations.

Among the most significant wildlife diseases, amphibian chytridiomycosis caused by the fungal pathogen Batrachochytrium dendrobatidis (Bd) has contributed to declines of hundreds of species worldwide [5]; but see [6]. In North America, notable Bd-associated declines have occurred across the west including the southern Rocky Mountains [7,8], Arizona and New Mexico [9,10], Nevada [11] and California [1214]. In several of these cases, infection outcomes varied widely among populations due to host-related and environmental factors including genetics, prior Bd exposure and abiotic conditions [1517].

For the stream-dwelling foothill yellow-legged frog, Rana boylii, Bd's role in the species' changing abundance across its endemic range (California and Oregon, USA) is not well-understood. The species has declined for at least the last half-century, with extirpations reported from xeric lower latitudes [18], at the wetter northern range limit [19] and downstream of large dams range-wide [20]. A mix of abiotic and biotic factors influence Bd infection risk and disease dynamics in many systems, including elevation, latitude, climate, habitat quality and host characteristics [21]. The relative importance of these factors remains unclear in rivers with winter flood/summer drought flow regimes typical across R. boylii's geographical range. Bd is considered a significant potential threat to R. boylii [22] because it is implicated in the species' disappearance from rivers of California's South Coast [23] and in recent autumn die-offs of R. boylii in Central Coast streams [24,25]. A large-scale assessment of Bd infections is needed to clarify how infections relate to historical declines in some regions' rivers and persistence in others, identify clusters of increased infection risk across the species’ range, and evaluate how infection incidence and severity changes with the seasonality of the Mediterranean climate and across the diverse ecoregions that R. boylii occupies.

Here, we leverage data from over 2000 field and museum samples covering 124 years to synthesize knowledge and evaluate patterns of Bd infections in R. boylii. We use a combination of modelling approaches and spatial scan statistics to ask: (i) how are Bd detections in R. boylii are distributed over space and time, (ii) whether watersheds with high versus low Bd infection risk clustered historically and today, and (iii) how Bd infections are related to biotic and abiotic factors. Our results highlight priority populations for Bd mitigation, regions that are data-deficient and warrant further sampling and monitoring, and remaining gaps in our knowledge about Bd susceptibility in R. boylii. Our study serves as a resource for wildlife managers implementing disease mitigation and species recovery projects, such as re-introductions, and as an example of collaborative research to address conservation challenges in wide-ranging imperilled species.

Figure 1.
Distribution of R. boylii samples assayed for Bd infection. Diamonds show museum samples (collected 1897–2005), circles show field samples (2005–2021). Filled symbols indicate Bd-positive samples. (a) Sampling locations across California and Oregon, USA. Symbols overlap in some localities; see inset barplots for sample sizes. Rana boylii clades are outlined and labelled, with California Endangered Species Act status abbreviated in parentheses: SSC = Species of Special Concern, TH = Threatened, EN = Endangered. (b) Spatio-temporal spread of Bd detections. Symbol size indicates sample size at the HUC-12 (sub-watershed) level. Generalized additive model (GAM) of latitude∼capture year + sample size in Bd-positive samples is shown with black curved line (R2 = 0.133).

Photo of R. boylii in Napa County, CA by Marina De León.
It must be thrilling for devotees of the putative divine malevolence to see the stunning success it is having exterminating so many species of frog, but one can't help but wonder what the ancestral frog did to incur this wrath. Did it maybe eat a forbidden mosquito or spawn out of wedlock?

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The Unintelligent Designer: Refuting The Intelligent Design Hoax

ID is not a problem for science; rather science is a problem for ID. This book shows why. It exposes the fallacy of Intelligent Design by showing that, when examined in detail, biological systems are anything but intelligently designed. They show no signs of a plan and are quite ludicrously complex for whatever can be described as a purpose. The Intelligent Design movement relies on almost total ignorance of biological science and seemingly limitless credulity in its target marks. Its only real appeal appears to be to those who find science too difficult or too much trouble to learn yet want their opinions to be regarded as at least as important as those of scientists and experts in their fields.

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The Malevolent Designer: Why Nature's God is Not Good

This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.

Illustrated by Catherine Webber-Hounslow.

Available in Hardcover, Paperback or ebook for Kindle


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Monday 26 February 2024

Unintelligent Design - How The Same Function Evolved Twice - Once in Vertebrates And Again in Insects


Diagram of an insect compound eye.

UC Irvine study shows similarities and differences in human and insect vision formation – UCI News

Regardless of the different structures in the compound eyes of insects and the eyes of vertebrates, at the heart of them both is a light-sensitive molecule, 11-cis-retinal, also known as 'visual Chromophore', but these are produced in two different ways from the same starting compound - β-carotene - which in humans is obtained from eating plants like carrots which are rich in Vitamin A from which β-carotene is derived.

This is one of those examples which are so common in biology, of where, had it been intelligent, the same designer could have used a process it had designed earlier but did not, instead it designed an even more complex way of doing the same thing, giving the lie to claims that the same 'intelligent' designer designed living things, insects and vertebrates have two different ways to achieve the same product - 11-cis-retinal; the second being the more complicated of the two.


Although the earliest vertebrates appeared about 518 million years ago, so predating the first insects by about 130 million years, the creationists dogma of omniscience which they traditionally ascribe to their putative designer god, would mean this alleged designer was already aware of the less complex way to make 11-cis-retinal, when if supposedly designed the vertebrate method.

Besides, creationist dogma also says they were all created on the same day - 10,000 years ago.

Wednesday 14 February 2024

Malevolent Design - Another Arms Race Between A Parasitic Worm And Its Host - Or is It Just Unintelligent Design?


Cane Toad, Rhinella marina
A secret war between cane toads and parasitic lungworms is raging across Australia

The subject of parasitic arms races throws creationists into a bout of cognitive dissonance from which they can only emerge with a hefty dose of double-think and self-deception, telling themselves that it's perfectly logical to hold two diametrically opposite and mutually contradictory views simultaneously, like believing that the term 'circle' describes a spere but the term 'square doesn't describe a cube.

They need to believe that, whilst it is central to their dogma and the belief on which all their god of the gaps and false dichotomy fallacies relies - that there is only one creator god capable of whatever it is they are waving as 'proof' or its existence, and at the same time believing that parasites were created by a different creator, over whom their omnipotent god has no powers and who goes toe to toe with it in parasite-host arms races.

Sadly for creationists, they were denied the argument concerning a second creator by their guru and Deception Institute flunky, Michael J Behe, who used the evolution of parasites like Escherichia coli and Plasmodium falciparum (the malaria parasite) as 'proof that their god is the intelligent designer behind the 'design' of all living things.

So, let's do what Behe unwittingly did and remove the second, evil designer from the equation, and see where it leads.

A case in point is the recently discovered arms race between the Australian cane toads and the lung worm parasite that infests their lungs:

Friday 9 February 2024

Unintelligent Design - The Heath Robinson Way Legumes Get Nitrates


Mechanism of Plants Obtain Nitrogen by Supplying Iron to Symbiotic Bacteria | Research News - University of Tsukuba

Creationism's 'intelligent' designer is nothing if not inventive. In fact, it's so inventive that it keeps on reinventing things it's already invented and designing new ways to do things it's already designed a way to do. It's almost exactly like it has no way of remembering what it did yesterday and using those designs and inventions today - a bit like a motor-car manufacturer who reinvents the wheel, or the steering mechanism every time it designs a new model.

Take, for example, the way most plants obtain the essential nitrates they need to make proteins. Nitrogen is abundant in the atmosphere (about 79%) where it exists as diatomic molecules N2, in which form plants can't assimilate it. Instead they depend on soil bacteria, the 'nitrogen-fixing' bacteria such as Azotobacter and Clostridium which convert N2, into ammonium (NH4+ which forms salts with other minerals in the soil, in which form it can be taken in through the roots of plants. Apparently, it was too simple to give plants the same metabolic pathways that the nitrogen-fixing bacteria have so they could make their own ammonium, so a more complex and less energy-efficient way to get nitrates into plants had to be invented.

A small amount of ammonia (NH3 is also produced by the action of lightening on atmospheric nitrogen and this, together with nitrates produced by industrial pollution is dissolved in rainwater and finds its way into the soil. Other bacteria, fungi and other soil organisms also release nitrates from decaying plant and animal matter in the soil.
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