Imaginative reconstruction of Novaculadon mirabilis. Likely this animal would have been a little larger than a mouse.
Picture credit: Hamzah Imran.
(L-R) Dr Roy Smith and University of Portsmouth student Ben Weston by the flint bed in Durlston Bay near Swanage, which is the layer of rock which the mammal fossil came out of.
When someone grows up being threatened with divine punishment for merely entertaining doubts about the literal truth of the Bible, it's hardly surprising that real-world evidence struggles to break through the psychological defences they've built to protect themselves. This phenomenon is what atheist author and philosopher, Professor Peter Boghossian refers to as doxastic closure — a mental state in which contrary ideas are shut out before they can even be considered.
Former young-Earth creationist and now science advocate and geologist Glenn Morton once described it as like having a “gatekeeper demon” perched on the edge of your consciousness—filtering out any facts or logical arguments that challenge creationist beliefs, while admitting only those misrepresentations of science that appear to support them.
In this mindset, inconvenient realities — such as the discovery of a 145-million-year-old fossil of an early mammal — are unlikely to dent the conviction that the Earth is only 6,000 to 10,000 years old, and that all animals were created in a single supernatural event. In this view, evolution is simply an illusion, no matter how well the evidence supports it.
Even so, for any creationist with the courage and intellectual honesty to read this far, the story of that inconvenient little fossil is well worth exploring. It was discovered by a palaeontology student from the University of Portsmouth, along the Dorset coast of England, and is the subject of a recent paper in Proceedings of the Geologists’ Association.
This find marks the first discovery of a multituberculate jaw at Swanage since Victorian times. Its distinct size and shape confirmed it as a completely new species.
An artist’s reconstruction of the fossilized landscape, plants and animals found preserved in a remote bonebed of Arizona’s Petrified Forest National Park
Illustration by Brian Engh
Reconstruction of life in Arizona, 200 million years ago.
Arizona’s Petrified Forest National Park is a place that many creationists might prefer to ignore—or misrepresent. It offers a vivid record of how life changed during the Triassic Period, between 252 and 201 million years ago. In other words, it documents the history of life in what is now Arizona during the vast stretch of time that predates the so-called “Creation Week,” as described in Bible-based creationist mythology.
In addition to the petrified remains of ancient conifers, the site preserves fossils of long-extinct crocodile-like reptiles and some of the earliest dinosaurs known from North America. Now, a new study of a fossil-rich bone bed from the late Triassic—around 09 million years ago—has revealed new insights into stream ecosystems of that time, including the discovery of the largest pterosaur yet found in North America.
Creationists frequently argue that macroevolution without divine involvement is impossible because it supposedly requires the creation of new genetic information to code for novel structures. They assert that such new genetic information cannot arise through natural processes, claiming this would violate the Second Law of Thermodynamics. However, try getting a creationist to explain what the Second Law of Thermodynamics actually is, how it relates to genetic information, and why it supposedly forbids gene duplication, and it quickly becomes apparent that they haven’t the faintest idea what they’re talking about.
Of course, this entire argument hinges on a distorted definition of macroevolution, namely the claim that it must involve the appearance of entirely new structures not present in ancestral forms. Like so many creationist arguments, it is built on misinformation and the misrepresentation of fundamental biological concepts. Macroevolution refers to evolutionary changes above the species level, while evolution more broadly is defined as a change in allele frequencies in a population over time.
Another familiar plank in the creationist propaganda platform is the patently absurd claim that evolution cannot occur through a loss of genetic information, on the grounds that lost genetic material is always deleterious—if not fatal—and therefore cannot be passed on to subsequent generations. This claim, too, wilfully ignores well-established mechanisms in evolutionary biology.
So, a recent paper from an international team including researchers from the University of Vienna and the University of Wisconsin–Madison (USA) should present a problem for that narrative. The study shows that the bizarre body plan of marine arthropods known as sea spiders (Pycnogonida) is the result of a lost gene.
If creationists were intellectually honest, they might take this as a cue to question why creationist ‘scientists’ (to use the term loosely) are misleading them. More likely, however, they’ll claim that it’s the mainstream biologists who are doing the lying—despite the fact that the latter group provide empirical evidence to support their conclusions.
Here we have yet another example demonstrating that, if we apply Discovery Institute fellow William A. Dembski's criteria for proving intelligent design — namely the presence of complex specified genetic information — then we must conclude that creationism's supposed intelligent designer is, in fact, a malevolent force devising ever more sophisticated ways to inflict suffering on the world.
Once again, honest creationists are left with a stark dilemma: either complex specified information is indeed evidence of design, in which case the designer is malevolent, or it is not, in which case a central tenet of Intelligent Design creationism collapses. The dishonest ones, of course, will simply dismiss the evidence, likely misrepresent the science, and continue to bear false witness against scientists. In neither case should we expect creationists to admit that the theory of evolution fully accounts for the appearance of "malevolent" design, arising naturally without conscious intent or divine interference.
It’s a curious paradox that people who claim to worship the God of the Bible as an omnibenevolent, anthropophilic being are so often willing to see that deity cast in the role of a malevolent agent—so long as they can reject the theory of evolution. This strongly suggests that their opposition to evolution is not primarily theological, but political.
The latest example comes from the tick-borne pathogen Anaplasma, which causes anaplasmosis and contributes to Lyme disease. This bacterium hijacks the cellular machinery of ticks to ensure its own survival and transmission to new hosts, including humans. Although Dembski has famously avoided providing a rigorous, testable definition of "complex specified genetic information," any such definition would surely encompass genetic adaptations that promote survival and reproduction.
What information do you have on Anaplasma and the tick that transmits it?
Anaplasma is a genus of bacteria that includes several species capable of causing disease in humans and animals. The most medically relevant species is Anaplasma phagocytophilum, which causes anaplasmosis—a tick-borne disease that affects both humans and various mammals.
Overview of Anaplasma
Anaplasma are obligate intracellular bacteria in the family Anaplasmataceae.
They primarily infect white blood cells (especially neutrophils in the case of A. phagocytophilum).
Disease is often seasonal, peaking during the months of high tick activity (late spring to early autumn in temperate zones).
In severe cases: respiratory failure, organ failure, neurological symptoms
Incubation period: ~5–14 days after a tick bite.
Treatment: Responds well to doxycycline, especially if started early.
If untreated, it can lead to complications, especially in the elderly or immunocompromised.
Tick Vectors
The primary vector in the United States is the blacklegged tick (Ixodes scapularis), also called the deer tick.
In Europe, the main vector is the castor bean tick (Ixodes ricinus).
These are the same ticks that transmit Lyme disease (Borrelia burgdorferi) and Babesia (babesiosis), leading to frequent co-infections.
Hosts and Reservoirs
Main animal reservoirs include:
White-tailed deer
Rodents
Small mammals
Ticks acquire the bacteria when feeding on an infected host and then transmit it during subsequent feedings.
Biological Strategy of the Pathogen
Recent research (such as the 2025 WSU referenced) shows that Anaplasmacan:
Hijack the tick's cellular defence mechanisms, particularly its oxidative stress response, allowing the bacteria to survive within the tick's gut.
Manipulate the cell death pathways of tick cells, suppressing apoptosis (programmed cell death) to extend the viability of the cells it infects.
Modify gene expression in the tick to enhance its own survival and transmission potential.
These mechanisms qualify as highly sophisticated biological strategies—precisely the sort of adaptations that Intelligent Design proponents would struggle to explain without appealing to either special pleading or malevolent intent.
Ecological and Public Health Impact
Geographic spread is increasing, partly due to climate change, which expands the habitat range of ticks.
Public health monitoring is challenged by co-infections and misdiagnosis (HGA is often confused with Lyme disease or viral infections).
Preventative strategies include tick checks, repellents, and public awareness campaigns.
Bacteria hijack tick cell defenses to spread diseaseWashington State University researchers have discovered how the bacteria that cause anaplasmosis and Lyme disease hijack cellular processes in ticks to ensure their survival and spread to new hosts, including humans.
Based in the College of Veterinary Medicine, the team found that the bacteria can manipulate a protein known as ATF6, which helps cells detect and respond to infection, to support its own growth and survival inside the tick. The findings, published in the journal Proceedings of the National Academy of Sciences, could serve as a launching point for developing methods to eliminate the bacteria in ticks before they are transmitted to humans and other animals.
Most research has looked at how these bacteria interact with humans and animals and not how they survive and spread in ticks. What we have found could open the door to targeting these pathogens in ticks, before they are ever a threat to people.
Kaylee A. Vosbigian, lead author
Department of Veterinary Microbiology and Pathology
College of Veterinary Sciences
Washington State University, Pullman, WA, USA.
Vosbigian and her advisor, Dana Shaw, the corresponding author of the study and an associate professor in the Department of Veterinary Microbiology and Pathology, focused their research on Ixodes scapularis, also known as the black-legged tick, which is responsible for spreading both Anaplasma phagocytophilum and Borrelia burgdorferi, the causative agents of anaplasmosis and Lyme disease. Both diseases are becoming increasingly common and can cause serious illness in humans and animals.
The team discovered that when ATF6 is activated in tick cells, it triggers the production of stomatin, a protein that helps move cholesterol through cells as part of a normal cellular processes. The bacteria exploit this process against their tick hosts, using the cholesterol — which they need to grow and build their own cell membranes but cannot produce themselves — to support their own survival and success.
Stomatin plays a variety of roles in the cell, but one of its key functions is helping shuttle cholesterol to different areas. The bacteria take advantage of this, essentially stealing the cholesterol they need to survive.
Kaylee A. Vosbigian
When the researchers blocked the production of stomatin, restricting the availability of cholesterol, bacterial growth is significantly reduced. The researchers believe this shows targeting the ATF6-stomatin pathway could lead to new methods for interrupting the disease cycle in ticks before transmission occurs.
As part of the study, Vosbigian also developed a new research tool called ArthroQuest, a free, web-based platform hosted by WSU that allows scientists to search the genomes of ticks, mosquitoes, lice, sand flies, mites, fleas and other arthropod vectors for transcription factor binding sites — genetic switches like ATF6 that control gene activity.
There aren’t many tools out there for studying gene regulation in arthropods. Most are built for humans or model species like fruit flies, which are genetically very different from ticks.
Kaylee A. Vosbigian
Using ArthroQuest, the team found that ATF6-regulated control of stomatin appears to be prevalent in blood-feeding arthropods. Since the hijacking of cholesterol and other lipids is common among arthropod-borne pathogens, the researchers suspect many may also exploit ATF6.
We know many other vector-borne pathogens, like Borrelia burgdorferi and the malaria-causing parasite Plasmodium, rely on cholesterol and other lipids from their hosts. So, the fact that this ATF6-stomatin pathway exists in other arthropods could be relevant to a wide range of disease systems.
Assistant Professor Dana K. Shaw, corresponding author.
Department of Veterinary Microbiology and Pathology
College of Veterinary Sciences
Washington State University, Pullman, WA, USA.
Significance
Infection dynamics for tick-borne pathogens like Anaplasma have primarily been studied in mammals. Comparatively less is known about tick–pathogen interactions. We found that Anaplasma activates the stress response receptor, ATF6, in ticks. Activated ATF6 functions as a transcriptional regulator. Using a custom script in R, we identified stomatin as an ATF6-regulated target that supports Anaplasma by modulating cholesterol trafficking. Our custom tool “ArthroQuest” revealed that the ATF6-regulated nature of stomatin is unique to arthropods. Given that lipid hijacking is common among arthropod-borne microbes, ATF6-mediated induction of stomatin may be exploited in many vector–pathogen relationships. In addition, our findings predict that there are many ATF6-regulated genes unique to ticks, highlighting that there is still much to be uncovered.
Abstract
How tick-borne pathogens interact with their hosts has been primarily studied in vertebrates where disease is observed. Comparatively less is known about pathogen interactions within the tick. Here, we report that Ixodes scapularis ticks infected with either Anaplasma phagocytophilum (causative agent of anaplasmosis) or Borrelia burgdorferi (causative agent of Lyme disease) show activation of the ATF6 branch of the unfolded protein response (UPR). Disabling ATF6 functionally restricts pathogen survival in ticks. When stimulated, ATF6 functions as a transcription factor, but is the least understood out of the three UPR pathways. To interrogate the Ixodes ATF6 transcriptional network, we developed a custom R script to query tick promoter sequences. This revealed stomatin as a potential gene target, which has roles in lipid homeostasis and vesical transport. Ixodes stomatin was experimentally validated as a bona fide ATF6-regulated gene through luciferase reporter assays, pharmacological activators, RNA interference transcriptional repression, and immunofluorescence microscopy. Silencing stomatin decreased A. phagocytophilum colonization in Ixodes and disrupted cholesterol dynamics in tick cells. Furthermore, blocking stomatin restricted cholesterol availability to the bacterium, thereby inhibiting growth and survival. Taken together, we have identified the Ixodes ATF6 pathway as a contributor to vector competence through Stomatin-regulated cholesterol homeostasis. Moreover, our custom, web-based transcription factor binding site search tool “ArthroQuest” revealed that the ATF6-regulated nature of stomatin is unique to blood-feeding arthropods. Collectively, these findings highlight the importance of studying fundamental processes in nonmodel organisms.
The North American deer tick, Ixodes scapularis, can transmit up to seven different pathogens that impact human and animal health including Anaplasma phagocytophilum (causative agent of anaplasmosis) and Borrelia burgdorferi (causative agent of Lyme disease) (1). The continuous rise in reported cases of tick-borne disease (2–10) underscores the need for novel intervention strategies. Although the intricacies of mammalian host–pathogen interactions have been well studied, comparatively little is known about tick–pathogen interactions.
Recently we have shown that A. phagocytophilum and B. burgdorferi activate the unfolded protein response (UPR) in ticks, which influences microbial colonization and persistence in the arthropod (11, 12). The UPR is a cellular response network that is initiated by three endoplasmic reticulum (ER) transmembrane receptors IRE1α, PERK, and ATF6. Each branch of the UPR initiates a signaling cascade and coordinates gene expression networks by activating specific transcription factors. We have shown that the IRE1α-TRAF2 pathway leads to microbe-restricting immune responses in arthropods by activating the NF-κB-like molecule, Relish (11). We have also demonstrated that stimulating PERK activates the antioxidant transcription factor, Nrf2, which facilitates pathogen persistence in ticks (12). Out of the three UPR receptors, ATF6 is the least understood (13). When activated, site-1 and site-2 proteases cleave the cytosolic portion of ATF6, which allows it to translocate to the nucleus and act as a transcriptional regulator (nATF6) (14). The role of ATF6 has never been explored in arthropod vectors.
Here, we demonstrate that Ixodes ATF6 is activated by tick-borne pathogens and supports A. phagocytophilum colonization in ticks. To determine how ATF6 impacts vector competence, we used protein modeling and a custom transcription factor binding site query to probe the ATF6 regulatory network in I. scapularis. Gene ontology (GO) and Reactome analyses identified Stomatin, a lipid homeostasis and vesical transport protein, as a potential gene regulated by ATF6 in ticks. Using pharmacological manipulations, RNA interference (RNAi), quantitative fluorescent assays, and immunofluorescence microscopy, we found that Stomatin supports pathogen colonization in ticks by facilitating cholesterol acquisition by the bacterium. These findings demonstrate that stomatin is induced during the arthropod-phase of the pathogen life cycle to enable survival and persistence in the vector.
Programs that predict transcription factor regulatory networks are generally restricted to model organisms, leaving out many arthropod vectors. We used our custom R script to develop a publicly available, web-based tool termed “ArthroQuest” that currently allows users to query 20 different arthropod vector genomes, in addition to Drosophila and humans. Queries with ArthroQuest revealed that the ATF6-regulated nature of stomatin appears to be unique to arthropods. Given that lipid hijacking and cholesterol incorporation is common in many arthropod-borne microbes (15), ATF6-mediated induction of stomatin may be a shared phenomenon among many vector–pathogen relationships that is exploited for the survival and persistence of transmissible pathogens.
This discovery poses a significant problem for proponents of Intelligent Design (ID) creationism because it challenges one of their core assertions: that complex specified information (CSI) within genetic material is a reliable indicator of an intelligent, purposeful designer. If we accept this premise, then we are compelled to ask why such intelligence would devote itself to crafting mechanisms that cause suffering, disease, and death—such as the ability of Anaplasma to hijack tick cell defences and ensure its own propagation at the expense of both ticks and mammalian hosts, including humans.
The usual ID response is to insist that their designer is benevolent — typically equated with the God of the Bible. But here, we are faced with a biological system so well-adapted to spreading infection that it must either be acknowledged as a product of evolutionary processes or attributed to a designer with malevolent intent. This is not a fringe example; it is one of many cases where nature reveals a level of intricate adaptation that ID advocates would normally cite as evidence for design, were it not so profoundly disturbing.
What this ultimately reveals is the theological inconsistency at the heart of ID creationism. The refusal to acknowledge the explanatory power of evolution, even when confronted with examples like Anaplasma, indicates that ID is not a scientific theory but a religious or ideological stance. The selective application of their own criteria — applauding "design" in butterflies but ignoring it in parasites — exposes the intellectual dishonesty behind the movement. Evolution, by contrast, provides a consistent and naturalistic framework that explains both the beautiful and the brutal features of the living world — without invoking a morally compromised designer.
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According to creationists, humans are the designer’s special creation, and the Universe, Earth, and all life upon it were created solely for our benefit.
If that were the case, one might reasonably expect human design to be uniquely perfect—free from disease and physical defects. Yet, paradoxically, we are more prone to cancer than our closest evolutionary relatives, the other great apes. Recent research from the UC Davis Comprehensive Cancer Center suggests that this heightened cancer susceptibility may be linked to the very mutation that enabled us to develop our comparatively large brains.
The theory of evolution, of course, precisely predicts these kinds of suboptimal trade-offs and their consequences. As an undirected, uncaring process, evolution is concerned solely with reproductive success—not with long-term health, perfection, or ideal design.
Intelligent (sic) Design creationists have painted themselves into a corner.
Two of their most prominent arguments—irreducible complexity (Michael J. Behe) and complex specified information (William A. Dembski)—are intended to demonstrate the involvement of an intelligent designer in the natural world. But when these same criteria are applied to harmful parasitic organisms, such as the common herpesvirus (cytomegalovirus), which is the leading infectious cause of birth defects in the United States, the implication is that this virus too is the product of intentional design by the same creator that ID proponents insist is responsible for all life.
Within the framework of Intelligent Design creationism, the conclusion is inescapable: their designer deity—typically equated with the omniscient, omnibenevolent god of the Christian Bible—knowingly and deliberately created a pathogen that causes immense suffering. If ID logic is followed consistently, their deity is not a benevolent creator but a malevolent force that engineers disease and deformity with full foreknowledge of the consequences.
The only escape from this theological and philosophical bind is for ID creationists to refute their own criteria—to claim that irreducible complexity and complex specified information are compelling proof of design when found in beneficial biological systems, but somehow irrelevant or invalid when found in destructive pathogens. In doing so, they are forced to hold two mutually exclusive beliefs simultaneously.
In reality, these hallmarks of design touted by ID advocates are common outcomes of natural evolutionary processes — especially arms races between host defences and parasitic invaders. These processes are inherently unguided and wasteful, which in itself refutes the idea of intelligent planning.
Another striking example of this evolutionary struggle has just been published in Nature Microbiology by researchers from the University of Pittsburgh School of Medicine and the La Jolla Institute for Immunology. Their study sheds light on how the herpesvirus has evolved sophisticated strategies to evade the immune system — a feature that ID logic would classify as evidence of "design."
Graphical representation of urea formation in a droplet.
Figure: Luis Quintero / ETH Zürich.
Creationism's ever-shrinking, gap-shaped creator god has just lost a little more ground. New research suggests that the formation of basic organic molecules may have been far easier under early Earth conditions than previously thought. Remarkably, scientists have found that urea—a key organic compound—can form spontaneously from ammonia and carbon dioxide on the surface of water droplets. This process requires no catalysts, no high pressure or heat, and consumes minimal energy.
Although vitalism was refuted as early as 1828 — decades before Darwin — creationists still claim that life cannot arise from non-living matter. Yet they quickly retreat when asked how dead food becomes living tissue, or what exactly they mean by ‘life’: a substance, a process, or some kind of magical force. In reality, life is a set of chemical processes, and at its core, it’s about managing entropy—using energy to maintain order against the natural drift toward disorder.
The discovery was made by researchers at Eidgenössische Technische Hochschule (ETH) Zürich in collaboration with colleagues from Auburn University in Alabama, USA. Their findings have just been published in Science.
The knee-jerk response from any creationist worth his or her salt, when shown evidence of observed instances of evolution, is to demand a redefinition of the term *evolution*—away from its scientific meaning of a change in allele frequency in a population over time, and towards the creationist’s caricature: a species instantaneously transforming into an entirely unrelated taxon. This is, of course, something evolutionary biologists have never claimed, and which—if it ever occurred—would actually refute the Theory of Evolution.
This is the all-too-familiar, disingenuous tactic of setting the bar impossibly high for one’s opponent, while keeping it at ground level for one’s own evidence-free superstition.
So, for those creationists more interested in finding workarounds to ease the cognitive dissonance between what they would like the facts to be and what science actually shows, than learning the truth about the world around us, the news that researchers at Chicago’s Field Museum have demonstrated evolutionary change in the city’s rodent populations over the last 125 years will likely present little difficulty. They can always chant, “But it’s still a chipmunk/vole/etc., so not evolution!”
However, for those with the intellectual integrity and humility to base their opinions on observable evidence, rather than dismissing any evidence that doesn't conform to their preconceived alternative reality, this finding is a compelling vindication of a basic principle of the Theory of Evolution: that species change over time in response to environmental pressures.
The researchers have recently published their findings in the journal Integrative & Comparative Biology.
Creationists have long misrepresented the so-called "Cambrian Explosion" as vindication of their belief in the spontaneous creation of complex multicellular life ex nihilo — as though organisms simply appeared, fully formed, without precursors. They portray it as an instantaneous event that defies evolutionary explanation, and falsely claim that it presents an insurmountable problem for evolutionary biology. In doing so, they even misquote the late Stephen Jay Gould, asserting that he admitted Darwinian evolution could not account for it and so invented the concept of "punctuated equilibrium" to paper over the cracks.
In a particularly striking display of cognitive dissonance, this version of events — supposedly occurring half a billion years ago — is frequently cited by the same creationists who insist the Earth is only 6,000 to 10,000 years old.
As is so often the case with creationist arguments, these claims are simply wrong. The Cambrian Explosion was not an instantaneous event, but a prolonged evolutionary process unfolding over some 10 million years, with evidence showing a transition from the static Ediacaran biota to the more mobile, complex organisms of the Cambrian. Gould, far from being an opponent of evolutionary theory, remained a staunch evolutionary biologist throughout his career. His now largely outdated concept of punctuated equilibrium was never an alternative to evolution, but rather an attempt to explain the appearance of abrupt change in the fossil record — a perception largely due to the compression of deep time in the geological column. When properly scaled, the fossil record easily accommodates the gradual evolution of complex traits.
Trace fossils are an indicator of the palaeoecological conditions in which the organism that generated them lived.
Now, new research by Olmo Miguez Salas of the University of Barcelona and Zekun Wang of the Natural History Museum in London has uncovered compelling evidence that pushes the roots of the Cambrian Explosion even further back in time. Their findings suggest that signs of mobility and bilateral body plans were already emerging within the Ediacaran biota. This extends the evolutionary runway leading into the Cambrian, giving more time for the radiation of novel body plans and for the development of evolutionary arms races—such as the emergence of predation, defence mechanisms, and sensory adaptations.
Their results are published in the journal Geology (paper here) and summarised in a news release from the University of Barcelona.
I sometimes imagine creationists hiding inside a bunker with no windows, completely cut off from the reality outside, where a torrential rainstorm is underway. From within their sealed refuge, they declare to themselves—and to the world outside—that there is no evidence of rain, simply because they can’t see any.
Their only source of information is a handful of picture books depicting a tropical paradise where it never rains, so they believe everything beyond their bunker must be warm and sunny—just as the picture books describe. Anyone who tells them otherwise, or tries to show them a different picture, must be lying to trick them.
How else can creationists be so insulated from the reality of the deluge of scientific evidence in the real world?
That slightly tortured analogy is by way of introducing another couple of scientific papers concerning the evolutionary divergence of the phenomenon of biofluorescence. Unlike bioluminescence—where light is produced by a physiological process using ATP and functions in total darkness—biofluorescence involves the absorption of ambient light, which is then re-emitted at a different frequency. Specialised proteins absorb this light energy, become unstable in their excited state, and return to their ground state by releasing photons—hence biofluorescence functions in low-light conditions.
Fish in particular, but also sea turtles and corals, use these glowing patterns as signals—for attracting mates, confusing predators, and more. According to two newly published papers by a team led by researchers at the American Museum of Natural History (AMNH), this phenomenon first emerged around 112 million years ago—once again, firmly within Earth’s long pre–'Creation Week' history. Since then, biofluorescence appears to have evolved independently up to 100 times, a clear indication of its adaptive benefits in dimly lit ocean environments.
Beyond the evidence for biological activity in a time creationists claim the Earth didn’t even exist, there's another uncomfortable detail for them: the researchers declare that to understand the pattern of bioluminescence in nature, “...we need to understand the underlying evolutionary story...” Not something a creationist, labouring under the delusion that biologists are abandoning the theory of evolution in favour of creationism, would want to read.
Unlike most of the palaeontology unearthed by science—which is often tens or even hundreds of millions of years older than Earth, according to creationist dogma—this discovery dates to a mere 5 million years ago. But the problem for creationists isn’t one of degree; it’s one of absolutes. If anything is older than Earth according to their doctrine, then that doctrine is simply wrong. It’s as straightforward as that.
Likewise, if even a single transitional or ancestral form exists, then the creationist insistence that such forms don't exist is demonstrably false.
Curiously, despite failing to grasp that binary logic, creationists continue to convince themselves that if they can cast doubt on even the tiniest detail of evolutionary science—perhaps a small gap in the fossil record or a question about a single species—then the entire edifice of modern biology collapses and “God did it!” triumphs by default, all without the faintest scrap of supporting evidence.
With that essentially childish view of how evidence and reasoning work, it will likely make no difference to their claims that a team of researchers from the Gray Fossil Site & Museum and East Tennessee State University (ETSU) have discovered the fossil of a comparatively large salamander dating back around 5 million years. This find sheds light on the explosive diversification of salamanders in what is now Appalachia some 12 million years ago. Today, Tennessee is home to about 50 species of salamander—roughly one in eight of all living species.
Researchers Ian Hawes of the University of Waikato and Marc Schallenberg of the University of Otago measure the physicochemical conditions of a meltwater pond.
Credit: Roger Summons
Pustular microbial mat section such as could have existend in small melt-water ponds.
Only by systematically ignoring geological and archaeological evidence can creationists continue to delude themselves into believing that Earth is just a few thousand years old and was perfectly created by an anthropophilic god especially for humans – its supposed “special creation.”
The evidence, however, paints a radically different picture from that childish superstition. Not only was Earth clearly not perfectly created for humans, it wasn’t perfectly created for any life form. And it is far older than creationists assert. In truth, around 600 million years ago, Earth was such a hostile place for life that it was entirely covered in ice. The polar ice sheets had extended until they met at the equator. These “Snowball Earth” conditions led to a mass extinction so severe that it remains something of a mystery how any life survived – especially complex eukaryotic cells.
Now, a multinational team of researchers led by scientists from the Massachusetts Institute of Technology (MIT) has found evidence that early life could have survived in small pools of surface meltwater. They reached this conclusion after studying similar meltwater pools on the McMurdo Ice Shelf in Antarctica. What they found not only showed that single-celled eukaryotes can survive in such conditions, but also revealed that the population of prokaryotes varies according to local environmental conditions
These meltwater pools act as microcosms of diverse environments and demonstrate how local factors shape the distribution of different species – exactly as predicted by the Theory of Evolution. Had the conditions been perfect as creationists insist, there could be no variation in the populations in these pools. Variation only arises because the species need to adapt to different conditions - something that would never be needed in perfectly designed conditions.
The human genome compacted inside cells eight hours after infection.
Credit: Esther González Almela and Álvaro Castells García
(Top) Cropped representative STORM-PAINT images of EdC-AF647 labeled hDNA (magenta), immunolabeled H3 (green), and their merge in mock and HSV-1 infected A549 cells. Scale bar: 2 µm. (Bottom) Zoomed-in regions are shown inside yellow boxes. Scale bar: 200 nm.
One of the many problems with Intelligent Design (ID) creationism is its complete failure to account for evolutionary arms races.
According to leading ID proponents like William A. Dembski and Michael J. Behe, living organisms and their parasites — including viruses — must have been intelligently designed because they are supposedly “irreducibly complex” and exhibit “complex specified information”. But if that were true, it would mean the same designer is deliberately crafting both parasites and the defence mechanisms their hosts use to fend them off — hardly the mark of a supremely intelligent creator.
A further problem, and one that creationists prefer to ignore, is theological: designing pathogens like viruses is fundamentally incompatible with the notion of a benevolent creator. In fact, it suggests a malevolent intelligence — one more concerned with maximising suffering than promoting life and maximising happiness. So, when science uncovers yet another example of a virus behaving with surgical precision and apparent ingenuity, ID creationists find themselves in a bind. Is irreducible complexity and complex specified genetic information not evidence of intelligent design after all? Or must they admit that the designer is, at best, morally indifferent — or worse, actively malevolent?
The latest headache for the ID camp comes courtesy of the Herpes simplex virus — the one responsible for cold sores. Researchers at the Centre for Genomic Regulation (CRG) in Barcelona, Catalunya, Spain, with colleagues in Guangdong Provincial People’s Hospital, Guangdong, China, have discovered that the virus can radically reorganise a host cell’s genetic architecture — and it does so using the host's own cellular machinery. Their findings have just been published open access in Nature Communications.
One of the enduring problems with the Denisovans has been the lack of substantial physical evidence. Although their existence was first confirmed through DNA analysis of a finger bone discovered in the Denisova Cave in Siberia, and genetic traces of interbreeding with Homo sapiens are widespread throughout Southeast Asia and Melanesia—suggesting a remarkably adaptable and far-ranging hominin—fossil evidence has remained frustratingly scant. Beyond the Siberian finger bone, we have only a few bone fragments from a cave on the Tibetan Plateau and a jawbone dredged up by fishermen off the coast of Taiwan. These scattered remnants were insufficient to assign a clear taxonomic identity, so the group remained simply ‘the Denisovans’.
That gap in the fossil record now appears to have been dramatically narrowed. A near-complete skull, dubbed the 'Harbin skull'—also known as 'Dragon Man' or Homo longi—has now been identified as belonging to a Denisovan. This remarkable specimen, found in northeastern China, may finally give the Denisovans a face and, by the conventions of biological nomenclature, the name Homo longi. Since it is the most complete and morphologically distinct fossil now associated with the group, Homo longi may become the formal species name, superseding the informal label ‘Denisovan’.
Of course, Denisovans pose an even greater challenge to creationist dogma than they ever did to palaeoanthropology. Their existence is fundamentally at odds with the belief that all humans descend from a single ancestral couple who committed the so-called Original Sin, for which redemption is supposedly possible only through accepting the mythologised sacrifice of Jesus. The evidence now shows not only that there was no original couple, but that there wasn’t even a single founding species. Modern non-African humans are the product of complex interbreeding events between at least three archaic human lineages—thousands of years before the Earth was allegedly created, according to young-Earth creationist timelines.
The identification of the Harbin skull as Denisovan has just been published by researchers from the Institute of Vertebrate Paleontology and Paleoanthropology in Beijing, China. Their findings appear in papers in Cell and Science, and in a news release from the Chinese Academy of Sciences Institute of Vertebrate Paleontology and Paleoanthropology.
