The venomous stinger of an Asian giant hornet (Vespa mandarinia). The venom injected by this stinger can cause sharp, intense pain as well as local tissue damage and systemic effects such as destruction of red blood cells and cardiac dysfunction, which may even be fatal.
Yes. As I’ve observed myself, the common pond frog eats wasps apparently with impunity. I once watched a frog in our garden pond consume three wasps within a few minutes as they came down to drink. These frogs have, of course, evolved in the presence of wasps.
Now, according to research by Shinji Sugiura at Kobe University, Japan, published today, open access, in the journal Ecosphere, frogs that have evolved alongside an even more dangerous member of the wasp family – the Asian giant hornet – have also evolved resistance to venom that is toxic, even lethal, to many other creatures.
Creationists, however, insist that evolution does not happen and that wasps, frogs, and hornets were all intelligently designed by a supernatural deity synonymous with the god of the Bible and Qur’an. This leaves us wondering why an allegedly omnipotent, omniscient, supremely intelligent designer would equip wasps and hornets with a sting to defend themselves against predators, only then to design predators with resistance to that sting.
Creationists normally ignore this question, of course. Even their stock excuse – 'The Fall' – cannot be applied here. Neither frog nor hornet is parasitic on the other, except in the trivial sense that any predator is a “parasite” on its prey. But in this case, the frog appears to be the beneficiary: it gains a meal at no cost, while the wasp or hornet loses its life. And it is difficult to imagine that the genes conferring this immunity do *not
fall within William A. Dembski’s definition of “complex, specified information”. If they do not, then nothing producing a beneficial outcome can be so classified, and his argument for the existence of an intelligent designer collapses.
As the outcome of an evolutionary arms race, both the sting and the resistance in frogs make perfect sense—no need to invoke some forgetful designer who cannot recall what it supposedly created yesterday and treats it as a problem to be solved today.
In the case of these frogs, there may even be two distinct forms of immunity: resistance to pain and resistance to toxicity. It is already known that some hymenopterans deliver an excruciating sting with low toxicity, while others deliver a highly toxic sting with little or no pain.
Scientists at the Institute of Science and Technology, Austria, have found that terminally ill pupae in an ant colony emit a chemical signal that prompts worker ants to disinfect them with formic acid — a process that also brings about their death. This behaviour helps keep the colony free from infection and represents a clear example of evolved altruism with a genetic basis. Their findings are reported, open access, in Nature Communications.
One of the criticisms often levelled at evolutionary biology is that it cannot explain altruism, since individuals that sacrifice themselves for others seemingly shouldn’t survive to pass on any genes responsible for such behaviour.
This is plainly untrue. Acts of altruism are widespread in nature: male spiders and mantises are consumed by their mates, providing nutrients for developing eggs; the offspring of social spiders consume their mother, then go on to consume one another. These behaviours persist because they enhance the success of the genes involved.
The key lies in what Richard Dawkins termed the selfish gene. Contrary to creationist misrepresentations, this is not a claim that there exists a gene for selfishness. It refers instead to the way genes appear to act in their own interests. Genes promoting altruistic behaviour benefit when that behaviour increases the reproductive success of individuals carrying the same genes — typically close relatives. The sacrifice of one carrier can thereby enhance the spread of the genes responsible for the altruism.
In humans, altruism arises not only from genetic evolution but also from memetic evolution — the inheritance and adaptation of ideas, norms, and cultural expectations. Human altruism rarely requires life-or-death sacrifice; it more often involves smaller acts such as sharing resources, giving up a seat on a bus, or letting another driver go first at a junction. The advantage, at both genetic and memetic levels, is that such behaviours help build societies where cooperation is reciprocated. Altruism is ultimately an investment in a more stable, supportive environment that may benefit the genes and memes of the individuals who contribute to it.
Researchers from Switzerland and Japan, led by Professor Yohei Yamauchi of Eidgenössische Technische Hochschule Zürich (ETH Zürich), have developed a microscopy technique that enables real-time, high-resolution observation of how a virus gains entry to a cell. Their findings are described in the Proceedings of the National Academy of Sciences of the USA (PNAS).
The process, in which a virus exploits the pathways cells normally use to take in larger molecules such as hormones, cholesterol, or iron, involves the active cooperation of the cell as it reaches out to engulf the viral particle. This mechanism is triggered by receptors on the cell surface, to which viruses bind while ‘surfing’ along the membrane, seeking regions rich in receptors to form a stable attachment.
In other words, creationists often portray this as an “irreducibly complex” system, supposedly dependent on all components being present from the outset, requiring what they call “complex specified information” in both virus and cell to produce the receptors and binding proteins. Discovery Institute fellows Michael J. Behe and William A. Dembski present this as evidence of intelligent design.
Their argument depends on a statistical sleight of hand: they treat the entire process as though it originated in a single event involving one cell and one virus, then calculate improbabilities for each step and multiply them together, producing a vanishingly small likelihood of the whole mechanism arising spontaneously. This ignores the fact that evolution operates in populations — often large ones — across long periods, where components accumulate gradually over generations, dramatically increasing the probability of multiple features emerging together in the same lineage.
It also overlooks the billions of years during which viruses and cells have co-evolved. As multicellular organisms evolved ever more sophisticated ways of receiving and responding to external signals and substances, viruses simultaneously improved their ability to exploit those mechanisms.
But to the scientifically illiterate target audience of the ID-creationism industry, evolution is imagined as a single event rather than a continuous process, leaving them oblivious to the misuse of probability and the underlying mathematical errors.
Creationists trying to use this argument for intelligent design usually respond to biologists pointing out the obvious fact that they just presented their putative god as some sort of celestial malevolence, by retreating into Bible literalism and religious fundamentalism and invoking mythical 'Fall', so betraying the claims of the Discovery Institute and its fellows that ID is real science, not bible-literalist creationism dressed in a lab coat, as a lie.
How influenza viruses enter our cellsFor the first time, researchers have observed live and in high resolution how influenza viruses infect living cells. This was possible thanks to a new microscopy technique, which could now help to develop antiviral therapies in a more targeted manner.
In brief
For the first time, a new high-resolution microscopy technique has allowed researchers to watch live as influenza viruses infect cells.
The international team led by ETH Zurich found that the cells actively promote virus uptake.
This technique could now help to develop antiviral therapies in a more targeted manner.
Fever, aching limbs and a runny nose – as winter returns, so too does the flu. The disease is triggered by influenza viruses, which enter our body through droplets and then infect cells.
Researchers from Switzerland and Japan have now investigated this virus in minute detail. Using a microscopy technique that they developed themselves, the scientists can zoom in on the surface of human cells in a Petri dish. For the first time, this has allowed them to observe live and in high resolution how influenza viruses enter a living cell.
Led by Yohei Yamauchi, Professor of Molecular Medicine at ETH Zurich, the researchers were surprised by one thing in particular: the cells are not passive, simply allowing themselves to be invaded by the influenza virus. Rather, they actively attempt to capture it.
“The infection of our body cells is like a dance between virus and cell.
Professor Yohei Yamauchi, corresponding author.
Molecular Medicine Laboratory
Institute of Pharmaceutical Sciences
Department of Chemistry and Applied Biosciences
Eidgenössische Technische Hochschule Zürich
Zürich, Switzerland.
Viruses surf on the cell surface
Of course, our cells gain no advantage from a viral infection or from actively participating in the process. The dynamic interplay takes place because the viruses commandeer an everyday cellular uptake mechanism that is essential for the cells. Specifically, this mechanism serves to channel vital substances, such as hormones, cholesterol or iron, into the cells.
Like these substances, influenza viruses must also attach to molecules on the cell surface. The dynamics are like surfing on the surface of the cell: the virus scans the surface, attaching to a molecule here or there, until it has found an ideal entry point – one where there are many such receptor molecules located close to one another, enabling efficient uptake into the cell.
Once the cell’s receptors detect that a virus has attached itself to the membrane, a depression or pocket forms at the location in question. This depression is shaped and stabilised by a special structural protein known as clathrin. As the pocket grows, it encloses the virus, leading to the formation of a vesicle. The cell transports this vesicle into its interior, where the vesicle coating dissolves and releases the virus.
Previous studies investigating this key process used other microscopy techniques, including electron microscopy. As these techniques entailed the destruction of the cells, they could only ever provide a snapshot. Another technique that is used – known as fluorescence microscopy – only allows low spatial resolution.
Combined techniques, including for other viruses
The new technique, which combines atomic force microscopy (AFM) and fluorescence microscopy, is known as virus-view dual confocal and AFM (ViViD-AFM). Thanks to this method, it is now possible to follow the detailed dynamics of the virus’s entry into the cell.
Video: Nicole Davidson / ETH Zurich.
Accordingly, the researchers have been able to show that the cell actively promotes virus uptake on various levels. In this way, the cell actively recruits the functionally important clathrin proteins to the point where the virus is located. The cell surface also actively captures the virus by bulging up at the point in question. These wavelike membrane movements become stronger if the virus moves away from the cell surface again.
The new technique therefore provides key insights when it comes to the development of antiviral drugs. For example, it is suitable for testing the efficacy of potential drugs in a cell culture in real time. The study authors emphasise that the technique could also be used to investigate the behaviour of other viruses or even vaccines.
Significance
Influenza A viruses (IAVs) continue to cause epidemics worldwide due to their high mutability. Nevertheless, the initial step of infection, viral uptake into cells, has been challenging to observe directly with conventional microscopy techniques. Here, we developed a hybrid imaging system combining atomic force microscopy and confocal microscopy with enhanced mechanical functionality and minimal invasiveness to directly visualize nanoscale dynamics of IAV and cell membranes during viral uptake into living cells. This system enables the analysis of IAV lateral diffusion resulting from IAV–membrane interactions and characteristic membrane morphological changes induced by IAV during endocytosis. Our approach offers a method to rapidly assess the impact of viral mutations on host cell entry, which is critical for understanding emerging IAV variants.
Abstract
Influenza A virus (IAV) entry into host cells begins with interactions between the viral envelope proteins hemagglutinin (HA)/neuraminidase (NA) and sialic acid moieties on the cell plasma membrane. These interactions drive IAV’s lateral diffusion along the cell membrane and trigger membrane morphological changes required for endocytosis. However, directly visualizing these dynamic processes, which are crucial for IAV entry, has been challenging using conventional microscopy techniques. In this study, we enabled live-cell observation of nanoscale morphological dynamics of IAV and the cell membrane by reducing the mechanical invasiveness of atomic force microscopy (AFM). A customised cantilever with less than half the spring constant of conventional cantilevers enabled virus-view AFM imaging that preserved IAV–membrane interactions. By combining virus-view AFM with confocal microscopy, we performed correlative morphological and fluorescence observations of IAV lateral diffusion and endocytosis in living cells. Variations in diffusion coefficients of single virions suggested heterogeneity in sialic acid density on the cell membrane. NA inhibition decreased diffusion coefficients, while reduced sialic acid density increased them. The timing of clathrin accumulation at virion binding sites coincided with a decrease in diffusion coefficients, a relationship that was maintained independent of NA activity or sialic acid density. As clathrin assembly progressed, ~100-nm-high membrane bulges emerged adjacent to the virus, culminating in the complete membrane envelopment of the virus at peak clathrin accumulation. Our virus-view AFM will deepen our understanding of various virus–cell interactions, facilitate the evaluation of drug effects and promote future translational research.
Influenza A virus (IAV) is an enveloped RNA virus with two key surface glycoproteins: hemagglutinin (HA) and neuraminidase (NA). The virus surface contains 300 to 400 HA and 40 to 50 NA molecules (1). IAV envelope proteins comprise at least 18 HA and 11 NA subtypes (2), which enable IAV to infect various host species including humans, birds, pigs, bats, and other animals (3). These envelope proteins play crucial roles in IAV infection of host cells.
They interact with sialic acids on cell surface glycolipids and glycoproteins (4) or with major histocompatibility complex class II (MHC class II) molecules (5–7). HA binds to sialic acids at the terminal ends of glycan chains on the cell surface. The HA–sialic acid interactions are inherently weak, with dissociation constants typically in the millimolar range (0.9 to 68.4 × 10−3 M) (8–10). However, multivalent binding of multiple HAs to sialic acids enables IAV to stably adhere to the cell membrane (11, 12). Meanwhile, NA catalyzes the cleavage of sialic acids (13), inhibiting stable adhesion of IAV to the cell membrane. Through these mechanisms, HA and NA effectively regulate the attachment and detachment of IAV to the cell membrane.
The competitive action between HA and NA allows IAV to diffuse laterally along the cell membrane surface topology (). This lateral diffusion represents a critical dynamic macroscopic phenomenon reflecting virus–membrane interactions. However, conventional microscopy techniques have struggled to detect IAV movement on the 10-nm-thick cell membrane, resulting in limited visualization success (15–18).
HA-NA-sialic acid interactions also trigger endocytosis involving morphological changes of the cell membrane. When diffusing IAV binds to functional receptors such as EGFR (19) and Cav1.2 (20) through sialic acids, it initiates the recruitment and assembly of the endocytic machinery including clathrin, actin, and dynamin. IAV utilizes multiple entry pathways including clathrin-mediated endocytosis (CME), macropinocytosis, and both clathrin-independent and dynamin-independent mechanisms (16, 21–23).
IAV primarily utilizes CME for cellular entry (16, 21). Previous imaging of membrane dynamics using atomic force microscopy (AFM) has revealed that in IAV-free CME, clathrin-coated membrane invaginations (pits) larger than 100 nm in diameter form (24, 25). This is accompanied by the emergence of actin-dependent membrane bulges that develop on one side of the pit and eventually lead to its closure. Although electron microscopy has provided morphological snapshots of pits during IAV internalization (26), the membrane dynamics during IAV internalization via CME have yet to be successfully visualized.
AFM enables mechanical imaging of sample morphology with nanometer-scale resolution (27, 28). Since the development of high-speed AFM in 2001 (29), this technique has contributed significantly to molecular dynamics analysis (30–36). Additionally, the advent of cell-imaging AFM in 2013 has enabled advances in membrane dynamics analysis (37, 38). The integration of cell-imaging AFM combined with confocal microscopy has provided unique capabilities for observing nanoscale membrane morphological changes in living cells (24, 25). Despite these advances, a major challenge persists: the mechanical interference of the cantilever with biological samples. Visualizing the dynamic processes of IAV lateral diffusion and internalization requires an innovative technology capable of simultaneously observing the nanoscale morphology of the 10-nm-thick cell membrane and the 100-nm spherical IAV interacting with cell surface sialic acid-bearing glycolipids and proteins. Given that multivalent IAV–membrane interaction forces are relatively weak, ranging from 10 to 25 pN (39), achieving low-invasive imaging capabilities is critical.
In this study, we address and overcome the challenge of mechanical interference by enhancing the low invasiveness of AFM through the use of a customised soft cantilever. In combination with confocal microscopy, low-invasive AFM enables simultaneous live-cell imaging of both morphology and fluorescence. The redesigned cantilever minimizes disruption of IAV–membrane interactions, allowing accurate observation of viral dynamics. Using this system, we investigated the lateral diffusion of single IAV particles under various conditions, including NA inhibition, reduced cell surface sialic acid density, and different viral subtypes. We also analyzed membrane morphological changes before and during IAV endocytosis. While fluorescently labeled IAV was primarily used, we also demonstrate our AFM’s capability to track unlabeled viruses. This virus-view dual confocal and AFM, called ViViD-AFM, enables correlative morphological and fluorescence imaging of IAV–membrane dynamics, providing nanoscopic insights into HA-NA-sialic acid interactions.
What ID advocates never seem to notice is that, in arguing that such mechanisms must have been deliberately engineered, they are attributing to their designer a system in which viruses are given exquisitely tailored tools for invading the very cells it supposedly created. If one insists that this is intentional design, then one must also accept that the designer crafted the molecular equivalent of lockpicks and battering rams, optimised for breaching living tissue. It is difficult to reconcile this with any notion of benevolence.
Indeed, by rejecting evolution as the explanation for viral entry, ID proponents corner themselves into an uncomfortable theological stance: their designer not only equipped viruses with the machinery to exploit cellular signalling, but also ensured that cells remained vulnerable to such exploitation. The result is an ecosystem in which suffering, disease, and death are not unfortunate consequences of natural processes but deliberate design choices.
This is, of course, why mainstream biology requires no such designer. Co-evolution naturally explains why cells have receptors essential for communication and nutrient uptake, while viruses have, over immense timescales, adapted to hijack those same pathways. No malevolent architect is required—only the simple, iterative logic of variation, selection, and replication.
Yet the ID movement persistently overlooks this simpler, evidence-based account, preferring instead an argument that—if taken seriously—presents their putative creator as either unable to prevent viral parasitism or fully complicit in engineering it. Neither option supports the benevolent, omnipotent designer they hope to defend.
Creationists and other religious fundamentalists claim that their god deliberately fashions each human life according to a divine plan — that every individual is personally designed, even down to the genes they inherit from their parents. But this raises a perpetually unanswered question: why produce so many sperm cells, all competing to reach the egg, if the outcome is pre-ordained?
Creationists also insist that our DNA is a “code”, equivalent to a computer program that must have been created by an intelligent designer or programmer.
If that were true, we would expect the genes bestowed on each individual to be robustly designed and immutable.
However, new research by scientists at the Centre for Genomic Regulation, Barcelona, Catalunya, Spain, just published in Nature Communications, shows that this is not the case — and once again, a prediction of fundamentalist creationism has been falsified by science.
The researchers found that the human genome is especially vulnerable to mutations in the first 100 base pairs of genes, particularly during the earliest rounds of cell division in embryo development. Each division introduces mutations with the potential to cause disease, including cancer. Because these mutations do not appear in every cell of the early embryo, the resulting individual becomes a genetic mosaic, with some cells and tissues carrying certain mutations while others do not. But if the mutated cells give rise to germ cells — eggs or sperm — the mutation can be passed to the next generation, whose members will carry it in all their cells and may develop disease as a result.
Unless creationism’s designer god intended this outcome, or is incompetent, there is no coherent way to present this as the deliberate work of an intelligent designer. It is, however, entirely consistent with an unintelligent, utilitarian evolutionary process that settles for sub-optimal solutions based on a single criterion: what produces the most descendants who themselves reproduce?
A recent study from the University of Leipzig, just published, open access, in Molecular Psychiatry highlights the difference between an intelligently designed system and one which evolved naturally. Change a single gene involved in neurotransmission and the human feature that creationists wave as evidence for intelligent design - the human brain - seriously malfunctions.
The gene, GRIN2A, encodes a key subunit of the NMDA receptor — a molecular gateway through the cell membrane of neurones essential for learning, memory, language development, and the ability of the brain to fine-tune its own wiring. When functioning normally, children learn to speak, form memories, and develop the balanced neural circuits that underpin thought and behaviour. When it doesn’t, the result can be epileptic seizures, speech loss, cognitive impairment, and an increased vulnerability to psychiatric illness. In some cases, even sleep becomes a time of neurological storm activity, with continuous spike-wave patterns eroding normal brain development.
For anyone who understands evolution, this fragility makes perfect sense. For those insisting that the human brain is the product of foresight and planning, it presents a serious problem. It is a system built by evolutionary tinkering, not design. The NMDA receptor is one of the pillars of excitatory communication in the brain. Yet it is also a precarious, expensive and failure-prone piece of biological machinery. A single amino acid substitution in the GRIN2A protein can derail synaptic signalling, scramble brain rhythms, or impair the processes that enable children to acquire language.
You would think that a planet designed specifically for humans would be safe—one with an abundant supply of clean water to drink and wholesome food to eat.
Sadly, that is far from the case. As recent research has shown, on top of the pathogens and parasites that abound in nature—and which seem almost purpose-built to cause suffering, not just to humans but to virtually every other life form—there now exists yet another threat. Wherever you look in the natural world, every species has one or more parasites adapted to live in or on it, and even parasites themselves often fall prey to their own parasites. To this long list we can now add a group of cyanobacteria capable of turning fresh water into a deadly neurotoxin during warm weather. It is almost as though Earth wasn’t designed by an intelligent, benevolent creator after all.
In science, this is what’s known as a falsified hypothesis. You begin with an idea—in this case, that Earth was designed for humans by an omnibenevolent, omniscient deity—then you consider what predictions would logically follow. One such prediction might be that a planet designed for human well-being would contain no natural hazards or harmful organisms that routinely inflict suffering. Then you examine the evidence. If the facts contradict the prediction, the hypothesis is falsified.
And that is precisely what the existence of harmful organisms does. The evidence directly contradicts the creationist claim of an intelligently designed planet optimally crafted for humans. This does not, in itself, disprove the existence of such a deity; rather, it falsifies the specific claim that the deity is all-loving and all-knowing, or that it intentionally designed Earth and its myriad pathogens and parasites. The alternative is that the god described in the Bible and Qur’an is not as advertised—or does not exist and played no role in designing the world. The pathogens and parasites appear to have arisen from entirely different processes while this supposed designer either looked away or was not involved at all. Such outcomes are not the work of a benevolent creator.
In fact, the deity’s reputation would fare better if it didn’t exist, because then it could not be held responsible.
Researchers at The Rockefeller University's Laboratory of Biochemistry and Molecular Biology have uncovered the mechanism that enables breast cancer cells not only to withstand environmental stress, but to turn it to their advantage. They have just published their findings in Nature Chemical Biology.
For ID creationists, these findings pose yet another challenge—one typically ignored or waved away as the consequence of ‘sin’, neatly exposing the Discovery Institute’s attempt to persuade US legislators and educators that ID is a genuine scientific alternative. No real science explains inconvenient evidence by invoking fundamentalist doctrine or unevidenced forces inherited from ancient superstition.
The Rockefeller University team has shown that breast cancer cells can override a regulatory factor that normally controls gene expression. The transcription of DNA into mature messenger RNA involves the enzyme RNA polymerase II (POL II), whose activity depends on around 30 subunits. One of these, MED1, normally carries acetyl groups. Without those acetyl groups, MED1 loses its ability to regulate POL II, allowing the enzyme to transcribe genes that help cancer cells survive. Environmental stress deacetylates MED1. In essence, conditions such as low oxygen or elevated temperature—deadly to normal cells—can instead make cancer cells more resilient.
Life reconstruction of Wadisuchus kassabi in Late Cretaceous Egypt, depicting an adult seizing a lungfish in a wetland while a juvenile looks on. The scene reflects the rich Quseir Formation ecosystem, complete with turtles and dense vegetation revealed by fossil evidence.
When scientists from Mansoura University, Egypt, recently announced in the Zoological Journal of the Linnean Society of London the discovery of an 80-million-year-old marine crocodyliform unearthed in Egypt’s Western Desert, the headlines hailed it as “the earliest known member of Dyrosauridae”, a forgotten branch of ancient crocodile-relatives adapted for coastal and marine life.
Found in mid-Campanian deposits of the Quseir Formation, Wadisuchus kassabi is represented by partial skulls and jaws from several individuals — enough to show that by this stage dyrosaurids already possessed the long, narrow snout and needle-sharp teeth suited for grabbing fish or turtles.
What makes this find so important is not merely the age — though pushing the dyrosaurid fossil record back by several million years is notable — but the evolutionary implications and what it tells us about the scientific method. The cranial anatomy of Wadisuchus exhibits a transitional mixture of primitive and derived features: reduced premaxillary alveoli, modified jaw-occlusion patterns, and dorsally positioned nostrils for surface-breathing, reflecting a transitional form on the path from earlier crocodyliforms toward specialised marine dyrosaurids. Phylogenetic analyses consistently recover Wadisuchus as the basal (earliest-diverging) dyrosaurid — pushing the origin and early diversification of the family deeper into the Cretaceous.
This discovery underscores a fundamental truth of modern science: claims are not fixed dogma, but provisional explanations always subject to revision in the light of new evidence. Just as Wadisuchus reshapes our view of when and where dyrosaurids emerged, other fossil finds have repeatedly nudged back the origins of major vertebrate lineages, re-drawn phylogenetic trees, or revealed unexpected ancestral forms. In this way the scientific method resembles nothing so much as a continual conversation with Nature — a conversation always open to challenge, refinement, or outright contradiction when the data demand it.
Unlike creationists, whom recent research has shown, believe not changing their mind is a sign of strength of character and commitment to their 'faith', scientists know that the real test of character is a willingness to accept the evidence and the humility to allow it to dictate opinion.
Incidentally, it might come as a shock to creationists that a marine fossil was found in the Sahara Desert and that Earth was not created as it just a few thousand years ago, but has changed significantly over the millions of years, including periods of 'green Sahara'. As someone who has flown in a small plane over the Egyptian desert, I can attest to the existence of dry riverbeds and feeder streams in that desert, even though today rain is almost unknown in the vicinity of Luxor.
56 million years ago, in that vast expanse of pre–‘Creation Week’ history when 99.975% of Earth’s story unfolded — long before creationists imagine the Universe even existed — an event occurred that gives the lie to the claim that their putative designer created Earth as a safe and stable planet, finely tuned for the existence of (human) life. Earth’s temperature rose by roughly 6 °C as the amount of carbon in the atmosphere increased dramatically.
The cause of this, the Palaeocene–Eocene Thermal Maximum (PETM), lay in the disruption of one of Earth’s major feedback systems. Plants sequester carbon through photosynthesis and lock it into their tissues, but that system was pushed out of balance until a new equilibrium eventually formed. It took some 70,000–100,000 years for the planet to recover.
The problem was that higher temperatures caused many plants to fail because they had evolved for cooler conditions, and evolution proceeds far too slowly to cope with rapid environmental change. As plant productivity collapsed, less carbon was sequestered, which in turn drove temperatures higher — a classic positive feedback loop, triggered by a relatively small initial shift.
The worrying parallel today is that the current rate of anthropogenic warming is around ten times greater than at the onset of the PETM.
How we know this — and how the PETM reshaped climate and the terrestrial biosphere — is explored in a paper by an international team of scientists, published open access (in unedited form) in Nature Communications.
Two of the authors have also written a summary of their research in The Conversation. Their article is republished here under a Creative Commons licence, with formatting adjusted for consistency.
56 million years ago, the Earth suddenly heated up – and many plants stopped working properly
Forest life in the Paleocene-Eocene Thermal Maximum
As we show in new research published in Nature Communications, one consequence was that many of the world’s plants could no longer thrive. As a result, they soaked up less carbon from the atmosphere, which may have contributed to another interesting thing about this prehistoric planetary heatwave: it lasted more than 100,000 years.
Today Earth is warming around ten times faster than it did 56 million years ago, which may make it even harder for modern plants to adapt.
Rewinding 56 million years
Plants can help regulate the climate through a process known as carbon sequestration. This involves capturing carbon dioxide from the atmosphere via photosynthesis and storing it in their leaves, wood and roots.
However, abrupt global warming may temporarily impact this regulating function.
Investigating how Earth’s vegetation responded to the rapid global warming event around 56 million years ago – known formally as the Paleocene-Eocene Thermal Maximum (or PETM) – isn’t easy.
To do so, we developed a computer model simulating plant evolution, dispersal, and carbon cycling. We compared model outputs to fossil pollen and plant trait data from three sites to reconstruct vegetation changes such as height, leaf mass, and deciduousness across the warming event.
The three sites include: the Bighorn Basin in the United States, the North Sea and the Arctic Circle.
We focused our research on fossil pollen due to many unique properties.
First, pollen is produced in copious amounts. Second, it travels extensively via air and water currents. Third, it possesses a resilient structure that withstands decay, allowing for its excellent preservation in ancient geological formations.
56-million-year-old fossilised palm pollen from the Bighorn Basin, Wyoming, United States.
Vera Korasidis
A shift in vegetation
In the mid-latitude sites, including the Bighorn Basin – a deep and wide valley amidst the northern Rocky Mountains – evidence indicates vegetation had a reduced ability to regulate the climate.
Pollen data shows a shift to smaller plants such as palms and ferns. Leaf mass per area (a measure of leaf density and thickness) also increased as deciduous trees declined. Fossil soils indicate reduced soil organic carbon levels.
The data suggest smaller, drought-resistant plants including palms thrived in the landscape because they could keep pace with warming. They were, however, associated with a reduced capacity to store carbon in biomass and soils.
In contrast, the high-latitude Arctic site showed increased vegetation height and biomass following warming. The pollen data show replacement of conifer forests by broad-leaved swamp taxa and the persistence of some subtropical plants such as palms.
The model and data indicate high-latitude regions could adapt and even increase productivity (that is, capture and store carbon dioxide) under the warmer climate.
A glimpse into the future
The vegetation disruption during the PETM may have reduced terrestrial carbon sequestration for 70,000-100,000 years due to the reduced ability of vegetation and soils to capture and store carbon.
Our research suggests vegetation that is more able to regulate the climate took a long time to regrow, and this contributed to the length of the warming event.
Global warming of more than 4°C exceeded mid-latitude vegetation’s ability to adapt during the PETM. Human-made warming is occurring ten times faster, further limiting the time for adaptation.
What happened on Earth 56 million years ago highlights the need to understand biological systems’ capacity to keep pace with rapid climate changes and maintain efficient carbon sequestration.
Vera Korasidis, Lecturer in Environmental Geoscience, The University of Melbourne and Julian Rogger, Senior Research Associate, School of Geographical Sciences, University of Bristol
Published by The Conversation. Open access. (CC BY 4.0)
Abstract
The Paleocene–Eocene Thermal Maximum (PETM) around 56 million years ago was a 5–6°C global warming event that lasted for approximately 200 kyr. A warming-induced loss and a 70–100 kyr lagged recovery of biospheric carbon stocks was suggested to have contributed to the long duration of the climate perturbation. Here, we use a trait-based, eco-evolutionary vegetation model to test whether the PETM warming exceeded the adaptation capacity of vegetation systems, impacting the efficiency of terrestrial organic carbon sequestration and silicate weathering. Combined model simulations and vegetation reconstructions using PETM palynofloras suggest that warming-induced migration and evolutionary adaptation of vegetation were insufficient to prevent a widespread loss of productivity. We conclude that global warming of the magnitude as during the PETM could exceed the response capacity of vegetation systems and cause a long-lasting decline in the efficiency of vegetation-mediated climate regulation mechanisms.
Rogger, J., Korasidis, V.A., Bowen, G.J. et al. Loss of vegetation functions during the Paleocene–Eocene Thermal Maximum. Nat Commun (2025). https://doi.org/10.1038/s41467-025-66390-8
Events like the PETM expose the fragility of the systems that sustain life and demonstrate how easily they can be tipped into new and often hostile states. Far from being the work of an infallible designer fine-tuning a planet for a single favoured species, Earth’s history shows a world continually shaped by feedback loops, chance events and the slow, directionless process of evolution. When those systems are pushed too far or too fast, life suffers — and it takes tens of thousands of years for the planet to recover.
What makes the comparison with today so stark is the rate at which we are forcing change. The PETM was a natural carbon-cycle disturbance that unfolded over millennia. Our own contribution has taken place in a geological instant, yet it is already driving shifts comparable in magnitude to that ancient warming pulse. If slow change overwhelmed ecosystems then, the acceleration humanity has produced is even more concerning.
Understanding the PETM is not simply an academic exercise. It is a reminder, written in deep time, that there are limits to what living systems can endure and that “business as usual” can push Earth into states incompatible with the world we inherited. The past cannot tell us exactly what will happen next, but it does show that the consequences of inaction are neither abstract nor remote. The warning signs are etched in the rocks; whether we heed them is up to us.
One thing we know is that there is no watching sky daddy who's going to come and rescue us from our folly.
Researchers at the University of Chicago have uncovered how prolonged exposure to ultraviolet (UV) radiation can lead to skin cancer by disabling a vital protective mechanism in skin cells. They have just published their findings, open access, in Nature Communications.
This protective mechanism relies on a protein called YTHDF2, which plays a key role in regulating RNA metabolism and maintaining cellular health. Sunlight degrades this protein, removing that safeguard and allowing damage to accumulate.
For advocates of Intelligent Design (ID) creationism, this research presents several awkward questions—questions they will either ignore or attribute to ‘sin’.
First, why is this protection needed at all? If life were intentionally and intelligently designed, why would RNA metabolism require an additional, failure-prone layer of regulation to keep cells functioning? Why not design it to be robust in the first place?
Second, why create a system so fragile that sunlight—an unavoidable feature of life on Earth—can disable it? Designing a repair mechanism that breaks down precisely when it is needed most hardly inspires confidence in the designer’s competence.
And then there is the broader problem: ID creationism equates its designer with the supposedly omniscient and omnipotent god of the Bible or Qur’an. If that is true, why design a mechanism that predictably causes cancer? Was this an act of malevolence or oversight?
If YTHDF2 were flawless and impervious to degradation, Discovery Institute fellow William A. Dembski would no doubt present it as an example of “complex specified information,” a supposed indicator of intelligent purpose. But its vulnerability raises uncomfortable possibilities: Is this an unsuccessful attempt to patch over earlier design flaws in RNA metabolism? A sign of competing designers beyond the control of ID’s putative omnipotent creator? Or evidence that the designer is actively introducing harm and suffering?
The answer, of course, is that this problem arises because the human body is not the product of intelligent design at all, but of a long evolutionary process that modifies existing processes and structures to produce workable—though often imperfect—solutions. Evolution favours whatever improves short-term reproductive success, even if it introduces compromises and sub-optimal outcomes that undermine long-term survival and health. These sub-optimal systems then drive the evolution of an additional layers of complexity to minimise the results of failure.
Like other organism's the human body is full of these examples of evolutionary compromises and sub-optimal solutions that cause diseases and health problems that illustrate the difference between an intelligently designed system and an evolved system. Looked at in detail, the human body is evidence against intelligent design and strongly supports the Theory of Evolution, as I show in my book, The Body of Evidence: How the Human Body Refutes Intelligent Design.
In 1858, Charles Darwin and Alfred Russel Wallace proposed the theory of evolution by natural selection, or as they described it, the origin of species by the preservation of favoured races. Darwin then elaborated on that central idea and concluded that the ‘tree of life’ would branch in ways consistent with diversification from common origins.
Creationists, on the other hand, claim all species were created by magic in their present form just a few thousand years ago, with no evolution and no common ancestry.
Darwin's Tree of Life sketch
Neither Darwin nor Wallace knew anything about DNA or genomes, or that mutations in DNA would become ‘favoured’ in particular environmental niches, driving diversification. They developed their ideas purely from the observable morphological and behavioural similarities and differences among species.
So, if the creationists are right, what should we see in these 1,000 genome sequences?
Here is something for creationists to run away from: why would a creator god who supposedly made the entire universe as a place for humans – especially American humans – to live, and arranged everything else for their benefit, create creatures in an environment so hostile that no human could survive there without specialised modern equipment? And how exactly did Noah collect two of each of the countless species that live there in great profusion, only to place them on the Ark and somehow maintain the extreme conditions they require?
The simple answer, as underscored by these discoveries, is that the whole tale is a childish fairy story. The organisms inhabiting the extreme conditions of deep-ocean trenches evolved to live there over millions of years, entirely independent of any usefulness to humans, whose existence is of supreme indifference to them.
The conditions described come from an open-access paper in Scientific Reports by an international team of oceanographers and marine biologists led by the GEOMAR Helmholtz Centre for Ocean Research in Kiel, Germany. They detail a unique environment 1,300 metres below the surface on a flank of Conical Seamount in the western Pacific, off Lihir Island in Papua New Guinea. What makes it unique is not simply that it is a hydrothermal vent, but that it is coupled with a cold methane seep from deep sediment layers. Hot, mineral-rich water and cold, hydrocarbon-rich methane gas rise along the same pathways, producing vent fluids filled with bubbles of cold methane.
The result is a unique ecosystem comprising dense fields of the mussel Bathymodiolus, along with tube worms, shrimp, amphipods, and striking purple sea cucumbers coating the rocks so completely that the underlying surfaces are entirely concealed.
Before methane-producing sediments accumulated, the hydrothermal fluids were even hotter, leaving behind tell-tale deposits of gold and silver, as well as antimony, mercury, and arsenic. The various lifeforms have adapted to thrive amid these chemicals, some of which are highly toxic.
Hydrothermal vents are among the most extraordinary environments on Earth — geochemical oases on the seafloor where life thrives without sunlight, fuelled instead by chemical energy. They overturn several once-assumed “rules” of biology and offer important clues about evolution, extremophiles, and possibly even the origins of life.~
Scientists led by the University of California, Riverside (UC Riverside) have identified a previously unknown form of DNA damage in mitochondria that may underlie a wide range of disorders linked to mitochondrial dysfunction. Their findings have just been published in the Proceedings of the National Academy of Sciences (PNAS).
Mitochondria contain their own DNA (mtDNA), which is essential for the proper functioning of these organelles that convert glucose into ATP, supplying cells with the energy needed to power metabolic processes.
The culprit is a large molecule, glutathionylate, which attaches to DNA and, if left unrepaired, can cause mutations. Researchers at UC Riverside, working with colleagues at the University of Texas MD Anderson Cancer Center, found that glutathionylated mtDNA accumulates in mitochondria at levels up to 80 times higher than in the cell nucleus. In short, the nuclear DNA repair system is vastly more efficient than its mitochondrial counterpart.
For advocates of Intelligent Design (ID), this discovery—if they understood it rather than dismissing it as part of an imagined conspiracy to undermine their faith—creates an acute theological problem. If we temporarily grant the core assumption of ID creationism, that a supernatural designer indistinguishable from the allegedly omniscient, omnipotent, and omnibenevolent god of the Bible and Qur’an is responsible for the design of mitochondrial DNA and its replication machinery, then only two coherent conclusions follow:
the designer is incompetent, having failed to produce fault-free mtDNA and an adequate repair mechanism, despite supposedly managing this for nuclear DNA; or
the designer could have produced fault-free mtDNA but chose instead to create error-prone mtDNA and a weak repair process, thereby intentionally designing disease and suffering—in other words, malevolence.
Moreover, the very need for a repair system betrays the absence of omnipotent, intelligent engineering. It is characteristic instead of the layered complexity produced by cumulative, unplanned evolutionary processes, which inevitably yield sub-optimal compromises.
The notion of an omniscient designer also rules out the excuse that the harmful consequences were unforeseeable. An all-knowing creator would have foreseen them; yet, according to ID logic, the designer implemented them regardless—designing mitochondrial DNA to fail and cause disease.
Thus, a biological phenomenon that fits seamlessly within the framework of evolutionary theory becomes an insurmountable theological obstacle for ID advocates, who must contort the evidence to suit a predetermined conclusion while catering to a scientifically illiterate and credulous audience.
Scientists at the University of California, Davis (UC Davis) have developed a strain of wheat capable of producing its own nitrate fertiliser, thereby increasing yields and reducing the amount of artificial nitrate that needs to be applied to fields. They achieved this by harnessing the nitrogen-fixing abilities of common soil bacteria that convert atmospheric nitrogen into nitrates in a form plants can absorb. Their research is published, open access, in the Plant Biotechnology Journal.
We seem to have been here before, observing how a food crop or domesticated animal could have been far more productive or better suited to human needs had it been given a more efficient “design” to begin with. In fact, virtually all our cultivated plants and domesticated animals have been profoundly reshaped by human selection, using the same biological principles as natural selection: favouring advantageous genes and eliminating those that are less so.
The new wheat strain produces nutrients that support anaerobic bacteria similar to those found in the root nodules of legumes such as peas and beans. These bacteria thrive in the low-oxygen environment of specialised nodules, where they fix nitrogen for the host plant. Wheat, however, lacks such nodules, and attempts to transfer nodule-forming genes from legumes have so far been unsuccessful. Instead, this new approach encourages nitrogen-fixing bacteria to live in close association with the wheat root system, effectively bypassing the need for nodules altogether.
This raises an awkward question for Intelligent Design creationists who equate their designer deity with the allegedly omnibenevolent, omniscient, omnipotent god of the Bible, Torah, and Qur’an. Why didn’t this deity simply give crops like wheat and other staple foods the genes the bacteria use, or at least give them the genes required to host nitrogen-fixing bacteria directly, rather than devising an unnecessarily complex symbiosis only some plants can use? And if, for some reason, these were impossible, why didn’t it create a system resembling the one now designed by the UC Davis researchers?
As with so much in nature that ID proponents like to cite as evidence of complexity—and therefore design—closer inspection typically reveals solutions that are suboptimal, needlessly intricate, and often wasteful. As I point out in my book, The Unintelligent Designer: Refuting The Intelligent Design Hoax, these are not hallmarks of intelligent engineering, which should aim for minimal complexity and maximal efficiency. Instead, they are entirely consistent with an undirected evolutionary process that tinkers with what already exists, with no foresight and with success measured solely by reproductive output.
The simple fact is that humans, using intelligence, can and do devise more efficient, sensible solutions than those found in nature—as the UC Davis team has demonstrated. Such solutions ought to have been obvious to any genuinely omniscient designer.
This leaves creationists with a stark dilemma: must they conclude that their designer god is incompetent, unable to anticipate future needs, or malevolent in withholding solutions that would benefit humanity? Or is it more plausible that these biological systems arose through the natural evolutionary processes they insist “don’t work”?
Advocates of Intelligent Design argue that all genetic information must originate from an intelligent agent, claiming that anything both complex and specified cannot arise without deliberate design. Their proposed designer is invariably indistinguishable from the god of the Bible and Qur’an: an all-knowing, all-powerful and supposedly benevolent creator.
What they never address is why a system attributed to such a being should fail at all—let alone in ways that cause profound suffering. It is akin to a human engineer producing an aircraft with engines that randomly fail or wings that detach mid-flight. And because this designer is held to be omniscient, the failure cannot be inadvertent. It must have been foreseen and deliberately incorporated, making such mutations part of the intended plan rather than unfortunate accidents.
Following the internal logic of ID creationism, Alzheimer’s dementia would therefore count as an intended outcome—meeting William Dembski’s own criteria for “complex specified genetic information”. This provides yet another instance, alongside the cancer example I discussed recently, of biological processes that appear designed to destroy. It sits comfortably among the many parasites and pathogens explored in The Malevolent Designer: Why Nature’s God is Not Good, all pointing to a distinctly malign pattern in the supposed “design”.
ID proponents typically fall back on blaming “The Fall”, implying the existence of another creative force beyond the control of their designer. This manoeuvre only further undermines their claim that ID is a scientific enterprise rather than creationism thinly disguised, since it relies on biblical literalism to rescue the argument from the conclusion of an incompetent or malevolent designer—an outcome that is theologically awkward and, for many believers, outright heretical.
Scientists led by Cold Spring Harbor Laboratory (CSHL) Professor Christopher Vakoc have uncovered a mechanism by which certain cancers manage to evade modern medical treatments: they can disguise themselves as ordinary cells from entirely different tissues, such as those of the skin. In two recent papers — one in Nature Communications and another in Cell Reports — Vakoc’s team identify the proteins that determine whether pancreatic cancer cells retain their pancreatic identity or slip into a skin-cell-like state. They also highlight a different set of proteins with a pivotal role in tuft-cell lung cancer.
Proteins, of course, are specified by genetic information, and if that information is altered, so too is the protein’s function. In the language of ID creationists, proteins are products of “complex, specified genetic information”.
This presents intelligent design creationists with a familiar problem — one they usually address, as with parasites and pathogens, by ignoring it and relying on the scientific illiteracy of their followers. If complex, specified information were genuinely evidence of an intelligent designer, then that same designer would be implicated in the origin of the proteins that maintain and diversify cancers. Their “specified information” is neither less complex nor less specific than the proteins involved in cognition, immunity, or embryonic development.
Only by refusing to define “complex specificity” in scientific terms — or to explain how it might be distinguished from information that is supposedly non-complex or non-specified — do ID advocates manage to maintain the fiction that all beneficial traits are the work of their designer, while harmful traits must arise from some other agency. This selective attribution, based entirely on subjective human preference, underscores the religious foundations of intelligent design creationism and its distance from genuine science.
Researchers have shown that kissing emerged early in the human evolutionary lineage, and that Neanderthals, along with other close relatives in our tangled family tree, almost certainly kissed as well.
Kissing is an intriguing behaviour, widely assumed to serve important social functions that outweigh the obvious drawbacks of exchanging microbes and viruses.
The team, led by Dr Matilda Brindle, an evolutionary biologist in Oxford University’s Department of Biology, based their conclusion on the principle that when two species on separate branches of the primate family tree share a behaviour, it was likely present in their common ancestor. This approach indicates that kissing arose among the ancestors of the great apes between 21.5 and 16.9 million years ago. Their findings were published very recently in the journal Evolution and Human Behavior.
Creationists who insist that evolutionary biologists are abandoning the Theory of Evolution—a framework on which this analysis directly relies—may be alarmed to find no evidence of such a retreat. Quite the opposite: the observation that a trait with both costs and benefits will persist when the benefits outweigh the costs neatly explains the evolutionary retention of kissing across several related species.
