For creationists, who typically know little or nothing about evolution and so have no understanding that it is a process that takes place in a population, not an event that happens to individuals, sexual reproduction is a fertile source of disinformation and misunderstanding with which to attack the Theory of Evolution.
For instance, they frequently argue that the probability of the 'first man' and 'first woman' evolving together is so highly unlikely that their myth of the spontaneous creation out of dirt of a man and the cloning of a woman by magic is a far more rational alternative explanation. The science is attacked because when they try to force fit their childish myth of every species having a single ancestral male and female couple into the science of evolution, it doesn't fit well. The possibility of the myth being wrong must never be contemplated, because that would risk having to change their mind.
However, science works by addressing questions, not by throwing stones at infantile straw-man parodies of alternative ideas and declaring victory by default.
For science, sexual reproduction presents evolutionary biology with a different long-standing puzzle. An asexual organism can pass on its entire genome without finding a mate, competing for one or investing energy in courtship. In species with separate sexes, there is also the familiar “twofold cost of males”: only females produce offspring, whereas every member of an asexual population can potentially reproduce.
All else being equal, an asexual lineage should therefore increase more quickly than a sexual one, and indeed there are a few examples of where this is true - a single female vine weevil can quickly populate a window box or plant pot with devastating consequences for the owner as I have found to my cost; a single marbled crayfish can rapidly spread through a new river system, out-competing any native species.
Yet sexual reproduction is widespread among eukaryotes and has persisted for hundreds of millions of years. This does not imply that evolution requires foresight or that sex was introduced by a designer for some future purpose. It means that, under many circumstances, the descendants of organisms that exchange and recombine genetic material must acquire advantages sufficient to offset the immediate costs.
One important advantage is that sex reshuffles the genome. In an asexual lineage, genes are inherited together as a largely indivisible package. A beneficial mutation can therefore carry neighbouring neutral or mildly harmful mutations with it as it spreads through a population—a process known as genetic hitchhiking. Sexual reproduction and recombination can break up these associations, separating advantageous mutations from some of the damaging evolutionary baggage accompanying them.
For most of its history, Earth was not a planet of trees, animals, fungi or anything else visible without a microscope. It was a microbial world. Life had existed for well over a billion years before the first clearly recognisable eukaryotic cells appeared in the fossil record, and for roughly another billion years after that, complex life remained comparatively inconspicuous.
That immense, slowly unfolding history is the subject of On the Hunt for Earth’s First Complex Life, an article in Universe Today by science journalist Bruce Dorminey, based on an interview with University of Oxford palaeontologist Associate Professor Ross Anderson. Anderson studies some of the most elusive fossils on Earth: the microscopic and usually soft-bodied remains of the organisms that preceded animals, plants and fungi.
The article is not a report of one new research paper, but an overview of an active field of research. Fortunately, several peer-reviewed studies provide the scientific background to Anderson’s comments. Together they describe not a sudden act of creation, but a long evolutionary transition from a biosphere dominated by bacteria and archaea to one containing eukaryotic cells, multicellular organisms and, eventually, animals.
From a Microbial World to Complex Life.
For most of Earth’s approximately 4.54-billion-year history, life was microscopic. The dates below represent the oldest reasonably secure evidence currently known, not necessarily the moment at which each evolutionary innovation first appeared. Any organism must have evolved before it could leave a fossil, and the earliest members of a lineage may have gone unpreserved or remain undiscovered.
Some major milestones
About 4.54 billion years ago — Earth formed. The young planet initially experienced intense volcanism, impacts and chemical evolution before stable oceans and environments capable of supporting life developed.
More than 3.5 billion years ago — microbial life was established. Ancient rocks preserve chemical and structural evidence of organisms that lacked nuclei and other membrane-bound organelles. Some proposed evidence is older, but its biological origin remains disputed.
By about 2.7–2.3 billion years ago — oxygenic photosynthesis had evolved. Cyanobacteria began using sunlight to extract electrons from water, releasing oxygen as a by-product.
About 2.4 billion years ago — the Great Oxidation Event. Oxygen began accumulating persistently in the atmosphere. This did not immediately produce complex life, but it profoundly altered ocean chemistry, mineral formation and the evolutionary opportunities available to organisms.
At least 1.75 billion years ago — recognisable eukaryotes. Organic-walled microfossils from northern Australia are among the oldest well-supported fossil eukaryotes. Their distribution indicates that they lived on or within oxygenated seabeds and probably already possessed mitochondria.
By about 1 billion years ago — multicellular eukaryotes. The fossil record contains increasingly persuasive examples of multicellular algae and other organisms in which cells were joined and organised. Multicellularity subsequently evolved independently in several eukaryotic lineages.
About 791 million years ago — diverse eukaryotes in the Svalbard sea. The Svanbergfjellet Formation preserves green algae and several enigmatic organisms with complex multicellular forms.
About 720–635 million years ago — Cryogenian global glaciations. During the “Snowball Earth” episodes, ice extended into tropical latitudes. The resulting environmental disruption probably caused extinctions while also creating new ecological opportunities after the ice retreated.
By about 574 million years ago — macroscopic Ediacaran organisms. Large, soft-bodied organisms appeared in marine ecosystems. Some may have been early animals, although the precise affinities of several famous Ediacaran forms remain debated.
From about 539 million years ago — the Cambrian radiation. Animal diversity, movement, burrowing, predation and biomineralisation expanded dramatically over millions of years. Skeletons and shells also made organisms much more likely to enter the fossil record.
How do scientists recognise a fossil eukaryote?
Finding a microscopic structure in an ancient rock does not automatically establish that it was alive, still less that it was a eukaryote. Palaeontologists first determine whether the object is genuinely biological, whether it was deposited with the surrounding sediment and whether it is as old as the rock containing it. They then examine combinations of features that are difficult to explain as mineral growths, later contamination or ordinary bacterial cells.
Size: Many early eukaryotic fossils are more than 100 micrometres across, considerably larger than typical bacteria. Size alone is not decisive, however, because some bacteria also produce exceptionally large cells.
Complex walls: Multiple wall layers, regularly arranged spines, sculptured surfaces and other elaborate structures indicate a degree of cellular control associated with eukaryotes.
Controlled openings: Some fossils have deliberately formed openings through which a cell apparently emerged from a resistant cyst. Their regular shape and position distinguish them from accidental tears or decay.
Internal structures: Preserved internal bodies, membranes or consistent patterns of cell division can support a eukaryotic interpretation, although claims that a particular structure represents a nucleus or organelle require especially strong evidence.
Multicellular organisation: Regular arrangements of connected cells, branching, differentiated regions or structures resembling holdfasts can demonstrate controlled growth rather than a chance aggregation of microorganisms.
Organic chemistry: Microscopy and spectroscopic techniques can establish that a fossil has a carbon-rich biological wall and reveal how heat, pressure and mineral reactions altered it after burial.
Geological context: Sedimentology and geochemistry reveal whether the organism lived in a coastal lagoon, on an oxygenated seabed or in deeper anoxic water. Finding the same form repeatedly within an appropriate environment strengthens its biological interpretation.
No single characteristic is necessarily conclusive. Large cells can be prokaryotic, mineral crystals can imitate biological shapes and geological alteration can create misleading structures. The strongest identifications therefore combine morphology, chemistry, repeated occurrence and environmental context.
Even when a fossil can confidently be identified as eukaryotic, its precise relationship to modern organisms may remain uncertain. Many organic-walled microfossils are consequently described by form rather than assigned prematurely to animals, plants, fungi or a particular group of protists. This caution is a strength of palaeontology, not a weakness: conclusions are calibrated to the evidence available and revised when better specimens or analytical techniques become available.
For creationists, the timescale alone is fatal. The rocks being examined are hundreds of millions to more than a billion years older than the entire Universe is supposed to be according to a literal reading of Genesis. More importantly, they preserve an ordered history of biological and environmental change that bears no resemblance to a six-day creation followed by a recent global flood.
The cellular innovation behind complex life
A eukaryotic cell is fundamentally more internally organised than a bacterial or archaeal cell. Its DNA is enclosed within a nucleus, while specialised compartments called organelles perform particular functions. Among the most important of these are mitochondria, which use oxygen to release energy from food and make energy-intensive forms of cellular organisation possible.
Certain bacteriophages found in the human gut have mutation hotspots scattered throughout their genomes that help them modify key defense genes, researchers report.
Credit: Sundharraman Subramanian and Alaina Pabbathi Cryo-EM Core Facility Michigan State University
One of the more persistent creationist falsehoods is the claim that mutations can only damage or destroy genetic information and can therefore provide none of the variation needed for evolution. The claim is usually protected from contrary evidence by leaving “information” conveniently undefined or by dismissing every beneficial mutation as merely a “loss of function”.
However, a new study by Jasper B. Gomez, Jeffrey E. Barrick and Christopher M. Waters of Michigan State University provides an especially clear demonstration of mutation generating heritable variation on which natural selection can act. Their findings were published in Nature Microbiology.
The researchers found that the genomes of the bacteriophages T2 and T4 — viruses that infect bacteria such as Escherichia coli — contain regions of repetitive DNA called contingency loci. These are mutational hotspots in which the DNA-copying machinery is particularly liable to slip while copying a run of repeated bases. It may insert or omit one of the repeats, changing the way the remainder of a gene is read and consequently altering the protein it produces.
Such replication errors occur in these regions thousands of times more frequently than mutations across the rest of the phage genome. Far from producing a population of genetically identical copies, therefore, phage replication continually generates a mixture of variants with different inherited characteristics.
The discovery arose from experiments involving a bacterial antiviral system called TgvAB, normally found in Vibrio cholerae, the bacterium that causes cholera. The researchers transferred the genes for this defence system into laboratory E. coli and exposed the bacteria to T2 phages. Although the defence initially restricted the phages, the viral population began overcoming it within hours.
A team led by scientists at Eurac Research, a private research centre based in Bolzano, South Tyrol, Italy, has reconstructed a remarkably detailed picture of the microbial community associated with Ötzi, the Copper Age man whose naturally mummified body emerged from melting ice high in the Ötztal Alps in 1991. Their findings, like so much relevant scientific evidence, are utterly incompatible with Bible-based creationist mythology.
According to young-Earth creationist dogma, the creator god committed an act of global genocide by drowning almost every terrestrial human and animal beneath a flood deep enough to cover the highest mountains. The precise date varies even among creationist organisations: Answers in Genesis places the Flood in 2348 BCE, while the Institute for Creation Research has calculated a date of about 2472 BCE. Both accept the claim derived from the Masoretic text of Genesis that the Flood occurred just 1,656 years after “Creation Week”, when everything was supposedly made from nothing by magic.
Several centuries before either of those proposed Flood dates, however, a man died at an altitude of about 3,200 metres in the Ötztal Alps. His body, clothing and equipment were preserved in a protected, icy hollow until melting ice exposed them in 1991, more than 5,000 years later. That man, now known as Ötzi or the Iceman, is still providing scientists with information about the life, health and microbial companions of a Copper Age European.
The Eurac-led team combined microbial cultivation with DNA sequencing and metagenomic analysis to distinguish between different components of the microbial community associated with the mummy. These included remnants of Ötzi’s original intestinal microbiome, microorganisms that colonised his body after death in the glacial environment, and modern contaminants introduced during more than three decades of museum conservation.
We’ve long suspected that the transition to farming and animal husbandry opened the door to a new era of disease – now DNA shows us that it happened at least 6,500 years ago,” says Professor Eske Willerslev, author of the new study.
Young Earth creationist mythology has it that sin, shortly after the magical creation of two adult humans, caused death and disease to enter the world. Until then, so we are expected to believe, there had been no disease and nothing ever died — not even, apparently, the plants Adam, Eve and the other animals ate.
Reality, of course, is materially different from the mythology produced by scientifically ignorant ancient pastoralists and later scribes who knew nothing of bacteria, viruses, parasites, epidemiology or evolution, and who interpreted misfortune in magical terms. Disease was not a supernatural punishment introduced at a single moment by a talking snake, a disobedient couple and an irritable god. It was, and remains, a biological process involving organisms evolving, spreading, adapting and, sometimes, crossing from one host species into another.
And the evidence now shows that at least 6,500 years ago, diseases were passing from animals into the humans who lived alongside them. The domestication of animals, the growth of settled farming communities and the rise of pastoralism brought humans, livestock, waste, parasites and pathogens into much closer proximity than before. This has long been thought to explain why humans suffer from so many infectious diseases. It is also a point Jared Diamond made in Guns, Germs and Steel: The Fate of Human Societies, where he argued that Eurasia’s abundance of domesticable animals, and Europeans’ long exposure to the diseases associated with them, helped Europeans to dominate other populations, often with their pathogens acting as an advance guard against peoples with no previous exposure or immunity.
That view of the zoonotic origin of many human diseases has now been strongly supported by the work of researchers led by Professor Eske Willerslev, of the University of Copenhagen and the University of Cambridge, in a study published open access in Nature in July 2025. The team analysed DNA from more than 1,300 prehistoric individuals, some up to 37,000 years old. Their bones and teeth provided an extraordinary archive of ancient microbial DNA, revealing traces of bacteria, viruses and parasites that infected humans across deep Eurasian history.
The results suggest that close cohabitation with domesticated animals, together with large-scale migrations of pastoralists from the Pontic Steppe, played a major role in the spread of zoonotic diseases. The researchers found that identifiable zoonotic pathogens first appear in their data from around 6,500 years ago, became more widespread after about 6,000 years ago, and peaked roughly 5,000 years ago — precisely the sort of pattern expected if lifestyle, animal husbandry, mobility and population contact were driving disease transmission.
This is especially awkward for creationists because the evidence does not point to a sudden, supernatural transformation of the world’s biology. It does not show disease appearing overnight as the result of a mythical “Fall”. Instead, it shows a long, historical and evolutionary process, unfolding through early Eurasian human history as changing human behaviour created new ecological opportunities for pathogens.
Clockwise: A bacterium retracts its pili, reeling in a piece of DNA in the environment. This action facilitates “natural transformation,” a process by which bacterium acquire new genetic traits, including antibiotic resistance.
Creationists have a problem of their own making. The same evolutionary processes they try to rebrand as evidence for a creator god are also the processes that produce parasites, pathogens and the molecular machinery by which they exploit their hosts. If Michael J. Behe wants to claim “irreducible complexity” as evidence of design, and William A. Dembski wants to claim “complex specified information” as the signature of an intelligent designer, then they cannot confine those arguments to the parts of biology they find theologically convenient. The same kinds of complexity and genetic information are also found in organisms that make us sick and increase the suffering in the world.
Although professional creationists, including fellows of the Discovery Institute such as Behe and Dembski, are careful to avoid naming their putative designer, their audience invariably identifies it with the supposedly omnibenevolent god of the Bible, Torah and Qur’an. But that creates an obvious problem: using their own criteria, this creator god must be credited not only with designing humans and other animals, but also with designing the bacteria, viruses, parasites and molecular mechanisms that infect, disable and kill them.
The significance of this is often lost on creationists because it requires a basic understanding of biology and a willingness to follow an argument to its logical conclusion. When they cite Behe’s favourite examples, such as the E. coli flagellum or anti-malarial drug resistance in Plasmodium falciparum, as evidence for their god, they are in effect crediting that god with designing mechanisms that help microbes move, invade, survive and evade our attempts to stop them. Point this out, however, and the same evidence that was allegedly scientific evidence for intelligent design is suddenly reinterpreted as evidence for “The Fall” and “Original Sin”. The pretence that creationism is science is abandoned in a hasty retreat into fundamentalist theology, where the same facts are repurposed to reach a more comfortable conclusion.
In addition to the two examples I recently discussed here and here, another example has now been reported — and this one involves a powerful molecular motor that should, by creationist standards, look very much like the sort of thing they would normally call “designed”. It is the type IV pilus retraction system, recently reported in Proceedings of the National Academy of Sciences of the USA (PNAS), which many bacteria use to retract tiny hair-like surface structures called pili. These pili act like microscopic grappling hooks, helping bacteria attach to surfaces and tissues, form antibiotic-resistant biofilms, and pull in fragments of DNA from their surroundings, including genes for drug resistance acquired from other bacteria.
Visible to the naked eye, fossilized bacteria or algae were found in an ancient seabed that emerged in the current Brazilian state of Mato Grosso do Sul
A paper in Gondwana Research, recently highlighted in a FAPESP press release, helps illustrate one of the great strengths of science and one of the fatal weaknesses of creationism as a means of discovering the truth.
It reports the results of a reassessment of microscopic fossil evidence from the late Ediacaran, previously interpreted as evidence of burrowing, worm-like animals — possibly the earliest known meiofauna, a type of tiny animal life otherwise securely associated with the Cambrian fossil record.
The earlier interpretation also carried a secondary implication: that oxygen levels in those late Ediacaran marine environments may already have been high enough to support active, motile, multicellular animals. That conclusion now looks much less secure, because the structures appear not to be animal burrows at all, but fossilised communities of algae and bacteria.
That is where the real lesson lies. One of the attractions of creationism is that it offers a spurious sense of certainty to people who value certainty more than truth and accuracy — the so-called “certainty embracers”. To them, the fact that science sometimes corrects itself, and that scientists change their minds when new evidence becomes available, is misrepresented as a weakness. Creationism, by contrast, is treated as an unchanging, eternal truth precisely because it is protected from correction by refusing to submit itself to evidence.
Religion offers unreasonable certainty; science works with reasonable uncertainty. The difference is that science is amenable to reason, evidence and correction, while creationism survives by rejecting them whenever they become inconvenient.
So creationists often seize on cases where one team of scientists re-evaluates evidence relied upon by an earlier team and concludes that the original interpretation was wrong. But this is not science failing; it is science working. It is exactly what makes science such a powerful tool for discovering what is true: it can change its collective mind when better evidence, better techniques and better analysis point in a different direction.
Sadly for creationists, however, this improved understanding rarely, if ever, turns out to support their beliefs. They may derive a few crumbs of comfort from the familiar refrain that “Darwinists got it wrong again”, but there can surely be little comfort in discovering that the structures in question were still made by living organisms some 540 million years before creationist dogma says Earth existed.
The corrected interpretation does not rescue creationism; it simply replaces one natural explanation with a better-supported natural explanation. The fossils are still ancient. They are still biological. They are still part of a deep-time history of life that creationism cannot accommodate without special pleading. The only thing that has changed is the identity of the organisms responsible for them.
The reassessment was led by Dr Bruno Becker-Kerber as part of his post-doctoral research at the Institute of Geosciences at the University of São Paulo (USP) and the Brazilian Center for Research in Energy and Materials (CNPEM), supported by a fellowship from FAPESP — Fundação de Amparo à Pesquisa do Estado de São Paulo, the São Paulo Research Foundation.
When working as a Senior Medical Research Technician for Oxford University, one of my pleasures on a sunny Summer day was to take a lunch break walking in the University Parks with colleagues, where we could watch first class cricket free, or, more interestingly, explore the ponds and banks of the Cherwell. Little did we know that almost 60 years later, an organism living in one of those ponds would yield up such compelling evidence that life is the result of an evolutionary process, with no evidence of divine intervention.
Creationists often cite the near-universality of the genetic code as evidence of a single designer using the same system for all life. Of course, the more obvious scientific explanation is common ancestry: all living organisms inherited the same basic translation system from a remote common ancestor, with later lineages modifying it in small but revealing ways. But even on creationist terms, the argument is a hostage to fortune, because if the same code supposedly points to the same designer, then differences in that code raise the obvious question: why would the same designer do the job in different ways?
That awkward question is neatly illustrated by research from the Earlham Institute, published in PLOS Genetics. The research concerns a single-celled ciliate, Oligohymenophorea sp. PL0344, found in a pond in Oxford University Parks, which has done something highly unusual with its genetic code. Codons that normally act as full stops in genes have been reassigned so that, instead of telling the cell to stop making a protein, they now code for amino acids.
This is not a trivial detail. The genetic code is the rulebook by which DNA and RNA sequences are translated into proteins. In most organisms, three particular codons act as stop signals, marking the end of a gene’s protein-coding sequence. Altering those signals might be expected to cause chaos, yet here is an organism in which evolution has tinkered with one of biology’s most fundamental systems and produced a viable alternative arrangement.
For creationists, this creates a familiar problem. The genetic code is invoked when it appears convenient to claim common design, but its exceptions are quietly ignored because they point instead to historical contingency, descent with modification, and evolutionary experimentation. Biology is not showing us the work of an omniscient engineer standardising a perfect system; it is showing us inherited systems being modified, repurposed and patched by evolution.
As every schoolboy knows, Alexander Fleming discovered the first antibiotic when the fungus Penicillium contaminated a Petri dish in which he had been culturing bacteria. What Fleming had discovered was a naturally occurring antibacterial substance produced by the fungus.
Such compounds are produced by fungi as part of their evolutionary arms race with the bacteria in their environment, and there is a whole range of them, many still awaiting discovery. On the other side of this arms race, bacteria evolve resistance.
It is a struggle that has been going on for hundreds of millions of years, ever since fungi evolved — and perhaps even earlier between ancestral eukaryotes and bacteria. Modern medical use of antibiotics has simply accelerated this ancient contest. We are now facing a major challenge in keeping pace with bacterial evolution, and hospitals in particular have become breeding grounds for resistant strains.
The tendency, therefore, is to assume that antibiotic resistance is a modern, anthropogenic phenomenon. It comes as something of a surprise, then, to learn that a bacterium, Psychrobacter SC65A.3, recovered from 5,000-year-old ice cores in a Romanian cave, has been found to be resistant to ten modern antibiotics.
Frankly, this is difficult to explain other than in terms of earlier evolutionary arms races. The discovery, by a team from the Institute of Biology, Bucharest, Romania, with colleagues from the University of Bucharest and the Universidad de Antofagasta, Chile, is reported in the journal Frontiers in Microbiology.
While this finding presents microbiologists with an intriguing puzzle, it presents creationists with a more acute problem. There simply should not be 5,000-year-old ice preserved in a Romanian cave — let alone viable bacteria within it — if the biblical narrative of a global flood some 4,000 years ago were historically accurate. And if a putative designer deity created bacteria already equipped with resistance to antibiotics that would not be synthesised by humans for millennia, that would imply pre-emptive malevolence.
This leaves modern Intelligent Design advocates with an uncomfortable choice: retreat into literalist theology and abandon scientific reasoning, or confront the implications of the evidence.
An open access paper in Proceedings of the National Academy of Sciences of the USA (PNAS) is a stunning example of the ludicrous complexity evolution has produced — the exact antithesis of what an intelligent designer would create, if such a designer were anything more than grossly incompetent. As I explain in my book, The Unintelligent Designer: Refuting The Intelligent Design Hoax, and as I have pointed out repeatedly on this blog, the hallmark of intelligent design should be minimal complexity and maximal efficiency. And yet what we find in humans — and in just about every other bilaterian animal with a gut — is a vast, intricate symbiotic microbiome supplying functions that could far more simply have been provided directly, with even a little forethought on the part of any competent designer.
Instead, in the sort of convoluted complexity that creationists like to attribute to their putative designer god, but which is in reality a hallmark of evolved systems, we see yet another example of a biological arrangement that betrays not intelligence, but its absence.
The paper, by an international team led by Professor Victor Sourjik and colleagues from the Max Planck Institute for Terrestrial Microbiology, the University of Ohio, and Philipps-University Marburg, describes how an interdependent gut microbiome helps to keep both the microorganisms and their host healthy. They show that this complex and dynamic community is governed by countless chemical interactions — not only among the microorganisms themselves, but also between microbes and host tissues. The perception of nutrients and signalling molecules by gut bacteria is therefore crucial in maintaining these relationships.
One key role of this microbiome is in deterring and combating pathological species which would otherwise find the gut — with its warmth and steady supply of pre-digested nutrients — an ideal environment to colonise. This must have been a problem even for the earliest animals with a digestive tract: a vulnerability effectively built into the body plan. The solution, in the form of beneficial commensal organisms, is therefore probably as old as the first tube-like bilaterians themselves.
The problem the human gut faces in this respect can be gauged from the fact that some studies have shown that 50-55% or more of the dry weight of human faces is bacteria, dead and alive[1] , with populations of bacteria in the order of 1011 bacteria per gram![2] Imagine then the opportunities this presents to a potentially pathological bacteria with a generation time in minutes. With a population exploding exponentially, the potential to overwhelm the host in a few days is enormous. This is the scale of the problem, and of the selection pressure to overcome it, that has produced this massively complex solution, because it wasn't solved in the initial 'design' stage.
Since it worked well enough, there has been no evolutionary pressure to replace it with a less vulnerable gut, or one better equipped to cope with infection without relying on an entire ecosystem of different microorganisms to maintain health. In other words, what we have today is the result of more than half a billion years of evolutionary history since this basic body plan first emerged in the Cambrian.
Researchers from the Hebrew University of Jerusalem have uncovered yet another layer of exquisite molecular sophistication in one of humanity’s most persistent and lethal parasites, Plasmodium falciparum, the chief cause of malignant malaria. Their findings, reported in a recent press release and published in the peer-reviewed Journal of Cell Biology, describe a newly identified regulatory “crown” checkpoint that controls parasite reproduction with remarkable precision.
It is difficult to imagine a discovery more awkward for Intelligent Design creationists, because Plasmodium falciparum is precisely the sort of organism that embodies everything Michael Behe and William Dembski insist cannot arise by evolution. Here is complex specified genetic information, tightly regulated developmental choreography, and interlocking biochemical machinery operating across multiple life stages — the very definition, we are told, of “irreducible complexity”.
Unfortunately for the Discovery Institute, this irreducible complexity does not produce a bird’s wing, a human eye, or some uplifting example of divine craftsmanship. It produces malaria — a parasite responsible for immense suffering and hundreds of thousands of deaths every year, mostly children. If complexity is meant to be a hallmark of intelligent design, then the designer’s portfolio includes some rather grim specialities.
The problem is compounded by the fact that Michael Behe has already made malaria central to his arguments. In The Edge of Evolution, he famously pointed to the parasite’s resistance to anti-malarial drugs as an example of the supposed limits of Darwinian evolution, claiming that multiple coordinated mutations were beyond the reach of natural selection. Yet malaria has since become one of the clearest demonstrations that evolution not only occurs, but does so rapidly and repeatedly, exploiting enormous population sizes and intense selection pressures to produce exactly the adaptations Behe claimed were improbable.
As Kenneth Miller pointed out, Behe's mathematical sleight of hand was to assume resistance had to evolve as a single event in a single cell, not across a large population over time - a fallacy of which any good microbiologists should have been aware.
This newly described “crown” stage is simply the latest reminder that biological complexity is not evidence of supernatural design. Evolution predicts complexity wherever it confers survival advantage — including in parasites, pathogens, and diseases. The only real surprise is that creationists continue to present complexity as a theological virtue, when nature so often deploys it in the service of exploitation rather than benevolence.
As ever, none of this will deter creationists from repeating their familiar articles of faith. Faced with an organism whose life cycle resembles a biochemical symphony — regulated checkpoints, specialised invasion machinery, host-cell remodelling, immune evasion, and reproductive stages split between mosquito and human — they will insist that this is not evidence for evolution but evidence against it. The argument, such as it is, runs that complexity must have been present from the start, because it could not have arisen gradually.
But this is simply the old “irreducible complexity” claim in a new disguise: the assertion that because creationists personally cannot imagine intermediate stages, no such stages could have existed. Science, of course, is not obliged to conform to the limits of anyone’s imagination. Evolution does not require that complex systems appear in a single leap. It proceeds by modification of what already exists — co-option, duplication, repurposing, and incremental refinement over deep time — producing the layered complexity we observe today.
Another common retreat is the insistence that this is merely “microevolution”, the trivial shuffling of genes within some mythical created “kind”. Yet Plasmodium falciparum is not merely adjusting the colour of its spots. It is evolving novel biochemical strategies, repeatedly acquiring drug resistance, fine-tuning developmental regulation, and exploiting host environments with extraordinary efficiency. If this is “only microevolution”, then the term has been drained of all meaning.
Microbiologists at the University of Southern California (USC) have discovered that one of Earth’s most abundant species, the SAR11 bacterium, has a fundamental — and potentially fatal — ‘design’ flaw. They have just published their findings in Nature Microbiology, and it should make grim reading for any creationists with sufficient courage to read it.
When you have trillions of copies, what does it matter to ‘selfish’ genes if a few billion go wrong and end up destroying the organisms they travel through time in? For an evolved organism, it matters not one tittle or jot to its genes, because they can always produce more copies. So long as there is a sufficiently large population to keep replicating, they will continue to exist and reproduce — and they have no other ultimate function. This is all they evolved to do.
But could we say the same for an organism designed by an omniscient, intelligent designer? What would be intelligent about creating an organism that, under particular but entirely predictable conditions, attempts to reproduce but succeeds only in making repeated copies of its DNA, fails to divide, and enters a runaway cycle of replication until it becomes so disorganised that it can no longer survive and effectively self-destructs?
SAR11 dominates the surface waters of the world’s oceans and accounts for around 40% of marine bacterial cells. As such, it is a vital component at the base of the marine food chain, and is so successful partly because of a process known as genetic streamlining — the evolutionary loss of genes to reduce energy demands in nutrient-poor environments. This alone is not the main problem for creationists to explain, although it does raise the obvious question of why a designer would burden an organism with a genetic load it does not need in the first place.
The real problem is that this streamlining, as an evolved process, comes at a cost. In shedding a load of mostly surplus genes, some essential ones are lost too — including genes that regulate the cell cycle. The result is a failure to divide after genome replication, with the cell instead entering an uncontrolled loop of DNA replication without division.
How on Earth can that be regarded as intelligent design? The organism does exactly what it is ‘designed’ to do under conditions of low nutrient stress, but in doing so falls into an inescapable trap. The consequence is that populations continue to decline even when nutrients later become available again — with potentially serious knock-on effects for other species higher up the food chain.
In a recent paper published in Biocontaminant, a group of environmental and public health scientists from China and the United States warn of the growing threat to public health from a group of dangerous free-living single-celled amoebae, the most notorious of which is Naegleria fowleri, also known as the brain-eating amoeba.
This complex, eukaryotic organism bears all the hallmarks of what Discovery Institute fellows William A. Dembski and Michael J. Behe insist is compelling evidence for intelligent design — complex specified genetic information and irreducible complexity — so, if we accept their argument, we have to conclude that whatever designer they imagine is doing this designing must also be the one who designed these nasty little ways to make people sick and die by having their brains eaten, like in some grotesque zombie apocalypse.
N. fowleri normally lives in soil and water, where it feeds on bacteria and other micro-organisms, but if it manages to get into a victim’s nose it can track along the olfactory nerves to the brain, where it treats brain cells the way it treats soil-borne organisms and sets about eating them. Infections are almost invariably fatal. What makes them particularly dangerous is their ability to survive extreme conditions that would kill most micro-organisms, such as high temperatures and strong disinfectants like chlorine, so they can persist in water supplies that most people regard as safe.
An additional hazard is that these amoebae can also act as carriers for other pathogens such as Legionella pneumophila, Chlamydia, and Mycobacterium tuberculosis. By providing these pathogens with protection from disinfection, the amoeba can enhance their pathogenicity and prolong their survival in the environment.
It would be hard to find a better example than N. fowleri of what creationists insist must be intelligently designed, so it follows that there are probably few better examples of the sheer malevolent evil of any designer of such creatures, from the perspective of the humans infected with it. For creationists to retreat into the traditional excuse of blaming ‘the Fall’ is to abandon the claim that irreducible complexity and complex specified genetic information are definitive evidence of intelligent design, and to retreat instead into religious fundamentalism and Bible literalism.
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.
Fig. 9: Schematic of microbial succession and biogeochemical processes in serpentinite mud at the Mariana forearc.
This schematic depicts lipid biomarker transitions from pelagic sediment communities to extremophiles adapted to high pH and redox conditions in serpentinite mud. The Mariana forearc biosphere is fueled by alkaline serpentinization fluids enriched in H2, CH4, DIC, and organic acids, sustaining specialized microbial communities. Lipid and stable carbon isotope data reveal a shift from relict methanogenic archaea, likely engaged in hydrogenotrophic methanogenesis, to a later ANME-SRB community mediating anaerobic oxidation of methane (AOM). Changes in substrate availability likely drove this transition. Distinct lipid signatures, including unsaturated diethers, acyclic GDGTs, and ether-based glycolipids, highlight adaptations to pH stress, phosphate limitation, and fluctuating redox conditions. The presence of in-situ branched GDGTs suggests previously uncharacterized bacterial communities persisting in these ultra-oligotrophic conditions. The Mariana forearc serpentinite biosphere, shaped by episodic fluid flow and substrate shifts, provides insights into deep-sea subsurface habitability. DIC = dissolved inorganic carbon, ANME anaerobic methanotrophic archaea, SRB sulfate-reducing bacteria, AOM anaerobic oxidation of methane, GDGT glycerol dialkyl glycerol tetraether.
Researchers at MARUM – Bremen University’s Centre for Marine Environmental Sciences – have made a discovery, just published open access in the journal Communications Earth & Environment, which, properly understood, should make depressing reading for creationists.
They have found living organisms both on and within the ocean floor, surviving in conditions where normal life would be impossible. These microorganisms inhabit mud volcanoes with a pH of 14, metabolising hydrogen and carbon to form methane by drawing energy from minerals in the surrounding rock. In other words, they live entirely without oxygen and with almost no organic matter, synthesising all they need from inorganic sources.
Informed creationists will recognise that these organisms directly refute their frequent assertion that life cannot arise from non-life — because producing life from non-life is precisely what these microorganisms are doing.
This also contradicts the biblical claim that all living things were created for the benefit of humans, since there is no conceivable way these organisms could serve any human purpose. Of course, to be fair, the authors of the Bible were completely ignorant of microorganisms, deep-ocean mud volcanoes, and chemosynthetic metabolism. They could only attempt to explain the larger creatures that lived in the limited region around their homes in the Canaanite hills.
And, as any informed creationist should also understand, these are exactly the sort of extreme conditions that biologists believe may have fostered the emergence of the earliest living organisms during the origin of life on Earth — once again undermining any claim that abiogenesis is impossible.
For an astonishing example of co-evolution — not just involving two organisms but a whole host that have co-evolved over millions of years — you need look no further than your own body, as a paper in *Frontiers in Neuroscience* by Erika L. English and James M. Krueger of Washington State University (WSU) shows. It reports the finding that sleep may be a co-evolved condition in which gut micro-organisms play a central role.
The researchers showed that, in mice, there is a close relationship between sleep patterns and the cyclical presence in the brain of a substance known as peptidoglycan (PG), normally found in the mesh-like walls of gut bacteria. Although co-evolutionary relationships are a well-established concept in evolutionary biology, this example illustrates just how intimate such relationships can become — to the point where it is difficult to say, in biological terms, which organism is the “product” of the other. To what extent are we the product of our gut bacteria, and to what extent are they the product of us?
Of course, creationism has nothing to say about this kind of co-evolution because the Bible is silent on the matter of micro-organisms or evolution. It contains nothing that wasn’t visible to its Bronze Age authors with the naked eye, or that lived outside the narrow confines of their limited experience. It was written by people with no appreciation of the history of life on Earth or of how it has been shaped by environmental change and ecological balances over deep time.
