Creationism Refuted - New Understanding of Modern Human And Neanderthal Interbreeding

Princeton geneticists are rewriting the narrative of Neanderthals and other ancient humans

The picture of modern human (Homo sapiens) interactions with Neanderthals (H. neanderthalensis) has just become significantly richer. New evidence reveals not just a single episode of contact within the last 50,000 years, but several waves of interaction spanning much of our species’ 200,000-year history.

It was previously believed that after our last common ancestor with Neanderthals and Denisovans split into separate populations around 600,000 years ago, one lineage remained in Africa and eventually evolved into H. sapiens by about 200,000 years ago. The other migrated into Eurasia and gradually diverged into Neanderthals in the west and Denisovans in the east, with limited contact between them. According to this model, modern humans left Africa around 60,000 years ago, encountered Neanderthals in Eurasia, and interbred with them shortly afterwards—about 40,000 to 50,000 years ago.

However, a new genomic analysis provides evidence for at least three distinct episodes of interbreeding. One occurred around 200,000 to 250,000 years ago—very early in the history of H. sapiens. Another took place about 100,000 to 120,000 years ago, long before the final major migration out of Africa, and the last around 40,000 years ago, as previously believed.

These findings suggest that there may have been multiple early migrations of H. sapiens into Eurasia, followed in some cases by return migrations back into Africa, before the final, successful dispersal around 60,000 years ago.

Some of the team’s evidence comes from detecting H. sapiens DNA in the Neanderthal genome, so these ingressions could have come from earlier migrations that then failed, leaving only their DNA in the Neanderthal population.

There are still unresolve questions about which species migrated out of Africa, when, and whether some, such as H. rhodesiensis, had a wide distribution across African and Eurasia with regional variants, so it is entirely possible that the earliest interactions with Neanderthals could have been between, say H. rhodesiensis which brought Neanderthal genes back into Africa and then interbred with diverging H. sapiens.

See the right-hand panel for an explanation of this so-called 'muddle in the middle'.

The study, led by researchers at Harvard University and Princeton University under the direction of Professor Joshua Akey of Princeton’s Lewis-Sigler Institute for Integrative Genomics, also supports the view that Neanderthals did not simply go extinct. Instead, their dwindling populations were gradually absorbed into expanding populations of modern humans.

Malevolent Design - What A Benevolent Designer Could Have Given Us, But Chose Not To, Apparently.

Coquerel's sifaka,Propithecus coquereli.

Ring-tailed Lemur, Lemur catta.

Study Suggests Lemurs Age Differently Than Humans | Duke Today

According to creationist superstition, humans were specially created by a perfect, anthropophilic, omnibenevolent creator god. If that were true, it would be reasonable to expect humans to be perfectly designed—free from defects or anything likely to cause long-term suffering.

However, the facts do not support this view. For example, as humans age, they increasingly suffer from a condition known as inflammaging — low-grade, chronic inflammation that contributes to a range of health problems, including heart disease, strokes, diabetes, cancer, and osteoarthritis.

Properly understood, this should give creationists cause for concern. The same designer god apparently gave some other primates—most notably, certain species of lemur—the ability to avoid this consequence of ageing. In fact, these lemurs even show a reduced tendency toward inflammatory conditions as they grow older.

This raises a serious question for Intelligent Design creationists: if the same designer god was capable of creating such a mechanism for lemurs, why did it not see fit to bestow the same gift upon its supposed favourite creation—humans? Or are these inflammatory conditions intended to cause suffering and disease as we age?

The discovery that some lemurs appear to have been specially favoured by a creator god—if we accept the ID creationist premise for the sake of argument—was made by a team of researchers led by Elaine Elizabeth Gomez Guevara, a biological anthropologist in the Department of Evolutionary Anthropology at Duke University, Durham, USA. As a scientist and biologist, however, she attributes the differences between lemurs and humans to evolution — not to indifference or malevolence on the part of a designer god.

The team has just published their findings in the Journal of Comparative Physiology B.

Creationism Refuted - How Evolving COVID-19 Is Making Creationism Sick

Simplified SARS-CoV-2 Evolutionary Tree

AI Generated image (ChatGPT4o)

News, in The Conversation that the latest variant of the Sars-CoV-2 virus that causes COVID-19, XFG, could soon become the dominant variant worldwide, prompted me to ask ChatGPT to construct a family tree for the known variants of the virus, to illustrate the basic principles of evolution that creationists continue to deny.

Construct a family tree of known SARS-CoV-2 variants and explain how this illustrates evolution in progress. Explanation: Evolution in Progress

This tree diagram represents a simplified phylogenetic tree of SARS-CoV-2, showing how the virus has evolved since it first emerged in Wuhan in late 2019.

Creationism Refuted - Evolution By LOSS of Genetic Information

Pycnogonum litoral, adult male feeding on a sea anemone.

C: Georg Brenneis

[Body]

Pycnogonum litorale, adult female feeding on a sea anemone.

C: Georg Brenneis

What the sea spider genome reveals about their bizarre anatomy

Creationists frequently argue that macroevolution without divine involvement is impossible because it supposedly requires the creation of new genetic information to code for novel structures. They assert that such new genetic information cannot arise through natural processes, claiming this would violate the Second Law of Thermodynamics. However, try getting a creationist to explain what the Second Law of Thermodynamics actually is, how it relates to genetic information, and why it supposedly forbids gene duplication, and it quickly becomes apparent that they haven’t the faintest idea what they’re talking about.

Of course, this entire argument hinges on a distorted definition of macroevolution, namely the claim that it must involve the appearance of entirely new structures not present in ancestral forms. Like so many creationist arguments, it is built on misinformation and the misrepresentation of fundamental biological concepts. Macroevolution refers to evolutionary changes above the species level, while evolution more broadly is defined as a change in allele frequencies in a population over time.

Another familiar plank in the creationist propaganda platform is the patently absurd claim that evolution cannot occur through a loss of genetic information, on the grounds that lost genetic material is always deleterious—if not fatal—and therefore cannot be passed on to subsequent generations. This claim, too, wilfully ignores well-established mechanisms in evolutionary biology.

So, a recent paper from an international team including researchers from the University of Vienna and the University of Wisconsin–Madison (USA) should present a problem for that narrative. The study shows that the bizarre body plan of marine arthropods known as sea spiders (Pycnogonida) is the result of a lost gene.

If creationists were intellectually honest, they might take this as a cue to question why creationist ‘scientists’ (to use the term loosely) are misleading them. More likely, however, they’ll claim that it’s the mainstream biologists who are doing the lying—despite the fact that the latter group provide empirical evidence to support their conclusions.

The research is detailed in an open-access paper in BMC Biology.

Malevolent Design - How Having a Bigger Brain Made Humans More Vulnerable To Cancer Than Our Chimpanzee Cousins

A Single Genetic Mutation May Have Made Humans More Vulnerable to Cancer Than Chimpanzees | Newswise

According to creationists, humans are the designer’s special creation, and the Universe, Earth, and all life upon it were created solely for our benefit.

If that were the case, one might reasonably expect human design to be uniquely perfect—free from disease and physical defects. Yet, paradoxically, we are more prone to cancer than our closest evolutionary relatives, the other great apes. Recent research from the UC Davis Comprehensive Cancer Center suggests that this heightened cancer susceptibility may be linked to the very mutation that enabled us to develop our comparatively large brains.

It’s almost as though the 'designer' either deliberately endowed humans with a cancer-promoting mutation or failed to anticipate the consequences of the so-called "complex specified genetic information" (© William A. Dembski / Discovery Institute) introduced to facilitate brain growth—and then neglected to revise the design when the flaw became evident. But, of course, being omniscient, we have to assume, if we accept creationists dogma for the sake of argument, it knew full well what the consequences of its design would be and designed them with that consequence in mind.

The theory of evolution, of course, precisely predicts these kinds of suboptimal trade-offs and their consequences. As an undirected, uncaring process, evolution is concerned solely with reproductive success—not with long-term health, perfection, or ideal design.

Creationism Refuted - Ancient DNA From Before Noah's Flood Shows Genetic Diversity

Final facial depiction of the Nuwayrat individual.

Morez Jacobs, A., Irish, J.D., Cooke, A. et al. (2025)

Geographic location of the Nuwayrat cemetery (red dot), and the previously sequenced Third Intermediate period individuals from Abusir-el Meleq (purple diamond).

Credit: Adeline Morez Jacobs.

Researchers sequence first genome from ancient Egypt | Crick

According to the biblical narrative, the entire human population of Earth was reduced to just eight related individuals around 4,000 years ago, following a global, genocidal flood — a flood which, curiously, left no trace.

Now, as is almost invariably the case, new scientific evidence is entirely inconsistent with that narrative. The genetic analysis of an individual who lived and died in Egypt between 4,500 and 4,800 years ago shows that he was approximately 80% North African, with the remaining 20% of his DNA tracing to the vicinity of Mesopotamia.

Historical evidence also shows that, long before the supposed global flood, agriculture-based civilisations had been established in both Egypt and Mesopotamia. These societies had already formed trading networks and cultural connections, and left behind artefacts — including stone structures and buried remains — which would have been completely obliterated by the kind of flood described in the Bible.

Pottery vessel in which the Nuwayrat individual was discovered.

Image: Garstang Museum of Archaeology, University of Liverpool.

More telling still is that, by 4,500 years ago, the human population — which, according to the biblical account, had only recently descended from a single family via incestuous inbreeding — had already diversified to the point that measurable genetic differences existed between the Egyptian and Mesopotamian populations. This diversity is what made such DNA analysis possible in the first place.

The analysis of this individual’s genome — the oldest Egyptian DNA recovered to date — was carried out by researchers from the Francis Crick Institute and Liverpool John Moores University (LJMU), UK. They have just published their findings, open access, in Nature.

Refuting Creationism - Confirmation of A Denisovan Skull - Homo longi

A reconstruction of Homo longi from the ancient Harbin skull found in China.

Image credit: John Bavaro Fine Art
Science Photo Library

Figure 1 The geographic locations and proteomic profiles for the Pleistocene hominin individuals with palaeoproteomic data.

The Middle Pleistocene cranium recovered in Harbin, Heilongjiang Province, northeastern China.

Key Evidence Links Harbin Individual's Nearly Complete Skull to a Denisovan--Institute of Vertebrate Paleontology and Paleoanthropology.

One of the enduring problems with the Denisovans has been the lack of substantial physical evidence. Although their existence was first confirmed through DNA analysis of a finger bone discovered in the Denisova Cave in Siberia, and genetic traces of interbreeding with Homo sapiens are widespread throughout Southeast Asia and Melanesia—suggesting a remarkably adaptable and far-ranging hominin—fossil evidence has remained frustratingly scant. Beyond the Siberian finger bone, we have only a few bone fragments from a cave on the Tibetan Plateau and a jawbone dredged up by fishermen off the coast of Taiwan. These scattered remnants were insufficient to assign a clear taxonomic identity, so the group remained simply ‘the Denisovans’.

That gap in the fossil record now appears to have been dramatically narrowed. A near-complete skull, dubbed the 'Harbin skull'—also known as 'Dragon Man' or Homo longi—has now been identified as belonging to a Denisovan. This remarkable specimen, found in northeastern China, may finally give the Denisovans a face and, by the conventions of biological nomenclature, the name Homo longi. Since it is the most complete and morphologically distinct fossil now associated with the group, Homo longi may become the formal species name, superseding the informal label ‘Denisovan’.

Of course, Denisovans pose an even greater challenge to creationist dogma than they ever did to palaeoanthropology. Their existence is fundamentally at odds with the belief that all humans descend from a single ancestral couple who committed the so-called Original Sin, for which redemption is supposedly possible only through accepting the mythologised sacrifice of Jesus. The evidence now shows not only that there was no original couple, but that there wasn’t even a single founding species. Modern non-African humans are the product of complex interbreeding events between at least three archaic human lineages—thousands of years before the Earth was allegedly created, according to young-Earth creationist timelines.

The identification of the Harbin skull as Denisovan has just been published by researchers from the Institute of Vertebrate Paleontology and Paleoanthropology in Beijing, China. Their findings appear in papers in Cell and Science, and in a news release from the Chinese Academy of Sciences Institute of Vertebrate Paleontology and Paleoanthropology.

Refuting Creationism - How Dogs Spread Across The Americas - Then Survived The Legendary Biblical Global Flood

Chihuahua dog in Mexico.

Credit: Urvashi9, Getty Images

Figure 1. Distribution of archaeological samples analysed in this study.

Manin, Aurélie, et al (2025)

Ancient DNA reveals new clues about the incredible journey of dogs in the Americas | University of Oxford

According to the Bible, all living things outside Noah’s Ark were destroyed once Noah, his family, and his chosen animals were safely sealed inside (Genesis 7:4). This supposedly happened around 4,000 years ago, according to the biblical narrative — which creationists firmly believe to be inerrant history.

The snag is, the evidence simply doesn’t support that timeline—or a global flood involving mass extinction by drowning. Not only would such a flood have left a distinctive global deposit of sediment, containing a chaotic mix of ancient and modern animal and plant species from disconnected continents, but it would also have erased all archaeological traces of earlier civilisations and palaeontological evidence of past life. In effect, it would have reset the clocks of both archaeology and palaeontology to start around 4,000 years ago.

Unfortunately for biblical literalists, that’s not what we see. The predicted tell-tale layer of silt is conspicuously absent. Instead, both archaeology and palaeontology reveal a pattern of uninterrupted occupation of the planet by animals and humans stretching back tens of thousands—and, in the case of animal and plant species, hundreds of millions—of years. For anatomically modern humans, there is a consistent archaeological record documenting their spread across all land masses (except Antarctica), during which they domesticated animals such as dogs, which migrated alongside them.

One example of this pattern — the migration of domestic dogs with humans into the Americas between 7,000 and 5,000 years ago — has just been published in Proceedings of the Royal Society B, by an international team of scientists led by Dr Aurélie Manin from the School of Archaeology at the University of Oxford. They have shown that all South American dogs prior to the arrival of Europeans, trace their ancestry back to a single female. One strain — the Mexican Chihuahua - still shows evidence of that ancestry.

Refuting Creationism - A 600-Million-Year-Old Common Ancestor of Cnidarians and Bilaterians.

Adult polyp of the sea anemone Nematostella vectensis.

Grigory Genikhovich

Bodybuilding in Ancient Times: How the Sea Anemone Got Its Back

Childish creationist claims of a young Earth, the spontaneous magical generation of all living organisms without ancestry, and the supposed absence of evidence for the evolution of life from a common ancestor have taken another blow with the publication of compelling new research that refutes these basic creationist dogmas.

An open access paper published in Science Advances describes a candidate ancestral mechanism for establishing bilaterality — symmetry along a central axis — in both bilaterians (animals with bilateral symmetry) and the sea anemone Nematostella. The study, conducted by four researchers from the Department of Neurosciences and Developmental Biology at the University of Vienna, provides crucial insights into the deep evolutionary origins of body plan organisation.

It is also clear from both the paper and the researchers' explanation in a University of Vienna press release that they regard the Theory of Evolution as essential to interpreting their findings. Their discovery fits squarely within the evolutionary framework and aligns with the established timeline for the diversification of animal life from a common ancestor.

What Is Bilateral Symmetry? Bilateral symmetry is a body plan in which an organism can be divided into roughly mirror-image halves along a single plane—from head to tail. Most animals, including humans, insects, and vertebrates, display this type of symmetry.

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Why Is It Evolutionarily Significant?

• Directional Movement: Bilateral symmetry enables streamlined, forward-facing movement—ideal for seeking food, mates, and avoiding danger.
• Cephalisation: This symmetry is often associated with the development of a head region where sensory organs and the brain concentrate—an evolutionary advantage for processing information efficiently.
• Complexity and Specialisation: It allowed for greater internal organisation and the evolution of specialised body systems (e.g., digestive, nervous, and circulatory).

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Evolutionary Milestone

Bilateral symmetry is thought to have evolved over 600 million years ago in a common ancestor of all bilaterians. This innovation marked a major turning point in the history of life, leading to the vast diversity of animal forms we see today.

Bodybuilding in Ancient Times: How the Sea Anemone Got Its Back

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New insights into the evolution of the back-belly-axis.

A new study from the University of Vienna reveals that sea anemones use a molecular mechanism known from bilaterian animals to form their back-to-belly body axis. This mechanism ("BMP shuttling") enables cells to organize themselves during development by interpreting signaling gradients. The findings, published in Science Advances, suggest that this system evolved much earlier than previously assumed and was already present in the common ancestor of cnidarians and bilaterians.

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Most animals exhibit bilateral symmetry—a body plan with a head and tail, a back and belly, and left and right sides. This body organization characterizes the vast group known as Bilateria, which includes animals as diverse as vertebrates, insects, molluscs and worms. In contrast, cnidarians, such as jellyfish and sea anemones, are traditionally described as radially symmetric, and indeed jellyfish are. However, the situation is different is the sea anemones: despite superficial radiality, they are bilaterally symmetric – first at the level of gene expression in the embryo and later also anatomically as adults. This raises a fundamental evolutionary question: did bilateral symmetry arise in the common ancestor of Bilateria and Cnidaria, or did it evolve independently in multiple animal lineages? Researchers at the University of Vienna have addressed this question by investigating whether a key developmental mechanism called BMP shuttling is already present in cnidarians.

Shuttling for development

In bilaterian animals, the back-to-belly axis is patterned by a signaling system involving Bone Morphogenetic Proteins (BMPs) and their inhibitor Chordin. BMPs act as molecular messengers, telling embryonic cells where they are and what kind of tissue they should become. In bilaterian embryos, Chordin binds BMPs and blocks their activity in a process called "local Inhibition". At the same time, in some but not all bilaterian embryonic models, Chordin can also transport bound BMPs to other regions in the embryo, where they are released again – a mechanism known as "BMP shuttling". Animals as evolutionary distant as sea urchins, flies and frogs use BMP shuttling, however, until now it was unclear whether they all evolved shuttling independently or inherited it from their last common ancestor some 600 million years ago. Both, local inhibition and BMP shuttling, create a gradient of BMP activity across the embryo. Cells in the early embryo detect this gradient and adopt different fates depending on BMP levels. For example, in vertebrates, the central nervous system forms where BMP signaling is lowest, kidneys will develop at intermediate BMP signaling levels, and the skin of the belly will form in the area of maximum BMP signaling. This way, the body's layout from back to belly is established. To find out whether BMP shuttling by Chordin represents an ancestral mechanism for patterning the back to belly axis, the researchers had to look at bilaterally symmetric animals outside Bilateria – the sea anemones.

An Ancient Blueprint

To test whether sea anemones use Chordin as a local inhibitor or as a shuttle, the researchers first blocked Chordin production in the embryos of the model sea anemone Nematostella vectensis. In Nematostella, unlike in Bilateria, BMP signaling requires the presence of Chordin, so, without Chordin, BMP signaling ceased and the formation of the second body axis failed. Chordin was then reintroduced into a small part of the embryo to see if it could restore axis formation. BMP signaling resumed—but it was unclear whether this was because Chordin simply blocked BMPs locally, allowing a gradient to form from existing BMP sources, or because it actively transported BMPs to distant parts of the embryo, shaping the gradient more directly. To answer this, two versions of Chordin were tested—one membrane-bound and immobile, the other diffusible. If Chordin acted as a local inhibitor, both, the immobile and the diffusible Chordin would restore BMP signaling on the side of the embryo opposite to the Chordin producing cells. However, only diffusible Chordin can act as a BMP shuttle. The results were clear: Only the diffusible form was able to restore BMP signaling at a distance from its source, demonstrating that Chordin acts as a BMP shuttle in sea anemones—just as it does in flies and frogs.

A shared strategy across over 600 million years of evolution?

The presence of BMP shuttling in both cnidarians and bilaterians suggests that this molecular mechanism predates their evolutionary divergence some 600-700 million years ago.

Not all Bilateria use Chordin-mediated BMP shuttling, for example, frogs do, but fish don't, however, shuttling seems to pop up over and over again in very distantly related animals making it a good candidate for an ancestral patterning mechanism. The fact that not only bilaterians but also sea anemones use shuttling to shape their body axes, tells us that this mechanism is incredibly ancient. It opens up exciting possibilities for rethinking how body plans evolved in early animals.

Dr. David Mörsdorf, first author
Department of Neurosciences and Developmental Biology
University of Vienna, Vienna, Austria.

We might never be able to exclude the possibility that bilaterians and bilaterally symmetric cnidarians evolved their bilateral body plans independently. However, if the last common ancestor of Cnidaria and Bilateria was a bilaterally symmetric animal, chances are that it used Chordin to shuttle BMPs to make its back-to-belly axis. Our new study showed that.

Grigory Genikhovich, senior author.
Department of Neurosciences and Developmental Biology
University of Vienna, Vienna, Austria

Publication:

David Mörsdorf, Maria Mandela Prünster, Paul Knabl, Grigory Genikhovich.
Chordin-mediated BMP shuttling patterns the secondary body axis in a cnidarian.
Science Advances (2025) 11(24). DOI: 10.1126/sciadv.adu6347

Abstract Bone morphogenetic protein (BMP) signaling patterns secondary body axes throughout Bilateria and in the bilaterally symmetric corals and sea anemones. Chordin-mediated “shuttling” of BMP ligands is responsible for the BMP signaling gradient formation in many bilaterians and, possibly, also in the sea anemone Nematostella, making BMP shuttling a candidate ancestral mechanism for generating bilaterality. However, Nematostella Chordin might be a local inhibitor of BMP rather than a shuttle. To choose between these options, we tested whether extracellular mobility of Chordin, a hallmark of shuttling but dispensable for local inhibition, is required for patterning in Nematostella. By generating localized Chordin sources in the Chordin morphant background, we showed that mobile Chordin is necessary and sufficient to establish a peak of BMP signaling opposite to Chordin source. These results provide evidence for BMP shuttling in a bilaterally symmetric cnidarian and suggest that BMP shuttling may have been functional in the potentially bilaterally symmetric cnidarian-bilaterian ancestor.

INTRODUCTION
Bone morphogenetic protein (BMP) signaling acts in secondary body axis patterning across Bilateria, and its functions as morphogen have been studied in diverse animal species (1, 2). The mechanisms of the BMP-dependent axial patterning are similar between arthropods and vertebrates, indicative of the shared origin of the secondary, dorsoventral axis in protostome and deuterostome Bilateria, a notion strengthened once broader phylogenetic sampling became available (2–7). Intriguingly, the same mechanisms appear to regulate the secondary axis patterning in the bilaterally symmetric cnidarian Nematostella vectensis, indicating that a BMP-dependent secondary body axis may have evolved before the evolutionary split of Cnidaria and Bilateria [(8, 9), reviewed in (1, 10)]. However, a scenario in which BMP-mediated secondary axes evolved convergently in Bilateria and bilaterally symmetric Cnidaria is also possible (2).

BMPs are secreted signaling proteins of the transforming growth factor–β superfamily frequently acting as heterodimers (11–13). Signaling through the BMP receptor complex (Fig. 1A) results in phosphorylation and nuclear accumulation of the transcriptional effector SMAD1/5, which regulates the expression of many crucial developmental transcription factors and signaling pathway components [(14–18), reviewed in (19, 20)]. BMP signaling is tightly controlled by a plethora of intracellular (14, 21) and extracellular regulators (22–29) of which Chordin (= short gastrulation in insects) is, arguably, the most famous one. Like many other secreted BMP antagonists, Chordin binds BMP ligands, blocks the interaction with their receptor, and thereby inhibits BMP signaling (30). However, Chordin can also have pro-BMP effects and promotes long-range activation of BMP signaling in Drosophila, Xenopus, sea urchins, and in the sea anemone Nematostella (7, 31–34). The phylogenetic distribution of Chordin and two central BMP ligands, BMP2/4 and BMP5-8, and their importance for the secondary axis patterning across phyla suggests that, during early animal evolution, these molecules may have represented the minimum requirement for the formation of the bilaterally symmetric body plan (2, 10). However, to evaluate such a possibility, we need to understand the “mode of action” of BMPs and Chordin outside Bilateria, and our model, the sea anemone Nematostella, allows exactly that.

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Fig. 1. Possible modes of action of BMP signaling during axial patterning in Nematostella.

(A) BMP signaling pathway. BMP dimers bind the heterotetrameric receptor complex, resulting in the phosphorylation of SMAD1/5. pSMAD1/5 forms a complex with the Co-Smad SMAD4, which regulates transcription in the nucleus. Chordin binds BMPs preventing them from activating the receptor complex. Metalloproteases like Tolloid and BMP-1 cleave Chordin and release BMP ligands from the inhibitory complex in Bilateria. (B) Expression domains of BMPs and BMP antagonists in an early Nematostella larva. Oral view corresponds to the optical section indicated with grey dashed line on the lateral view. Pink circles show the nuclear pSMAD1/5 gradient. (C) The shuttling model suggests that in Nematostella, a mobile BMP-Chordin complex transports BMPs through the embryo. Receptor binding is inhibited in cells close to the Chordin source due to high concentrations of Chordin. On the opposite side of the directive axis, BMPs bind their receptors and activate signaling upon release from Chordin. Tolloid might be involved in the cleavage of Chordin and release of BMPs from the complex with Chordin also in Nematostella. (D) In the local inhibition model, Nematostella Chordin acts locally to inhibit BMP signaling and promote the production of BMP2/4 and BMP5-8 mRNA. Chordin mobility is not required for asymmetric BMP signaling.

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BMP signaling in Nematostella becomes detectable during early gastrula stage in a radially symmetric domain: The phosphorylated form of the BMP signaling effector SMAD1/5 (pSMAD1/5) is detected in the nuclei around the blastopore (14, 35). Shortly after the onset of BMP activity, the radial symmetry of the embryo breaks, establishing the secondary, “directive” body axis with minimum BMP signaling intensity detectable on the side of BMP2/4, BMP5-8, and Chordin expression and maximum BMP signaling on the side opposite to it (Fig. 1B) (14, 34, 35). The symmetry break occurs despite the fact that mRNAs of the type I BMP receptors Alk2 and Alk3/6 and the type II receptor BMPRII are maternally deposited (36) and remain weakly and ubiquitously expressed in the embryo (fig. S1) gradually developing a slight bias toward the “high pSMAD1/5” side of the directive axis by early planula stage (14). BMP2/4 and BMP5-8 are co-expressed in the late gastrula/early planula, and both these ligands are crucial for BMP signaling and directive axis patterning because knockdown of either ligand abolishes pSMAD1/5 immunoreactivity and completely radializes the embryo (34). Individual knockdowns of either BMP2/4 or BMP5-8 result in a strong up-regulation of transcription of both BMP2/4 and BMP5-8 in a radially symmetric domain showing that both these genes are negatively controlled by BMP signaling. Despite transcriptional up-regulation of BMP2/4 in BMP5-8 morphants and BMP5-8 in the BMP2/4 morphants, no nuclear pSMAD1/5 is observed in such embryos (9, 34, 35), suggesting that BMP2/4 and BMP5-8 signal as an obligate heterodimer during axial patterning in Nematostella.

The “core” BMPs, BMP2/4 and BMP5-8, are not the only BMP ligands present in the embryo at this stage. GDF5-like (GDF5L) is a BMP ligand expressed on the side of strong BMP signaling (Fig. 1B). GDF5L expression is abolished in the absence of BMP2/4 and BMP5-8, and the role of GDF5L appears to be in steepening the pSMAD1/5 gradient making it a “modulator” BMP (14, 34, 37). The BMP signaling gradient is stable over many (>24) hours during which it patterns the directive axis (9, 14, 34, 35, 37). Considering the short half-life of phosphorylated SMAD1/5 reported in other systems (15, 21), this indicates that long-range transport (~100 μm) of BMP2/4 and BMP5-8 and constant receptor complex activation is necessary to maintain BMP signaling. How it exactly happens that the core BMP ligands, BMP2/4 and BMP5-8, are expressed on one side of the embryo and the peak of BMP signaling activity is on the opposite side is currently unknown.

One possible explanation involves Chordin-mediated shuttling of BMP ligands, described in the dorsoventral patterning in Drosophila and Xenopus (7, 34, 38). In this model, Chordin inhibits BMP function locally, close to the Chordin source cells, but promotes long-range BMP signaling by forming a mobile complex with the BMP dimer, which is released once Chordin is cleaved by the metalloprotease Tolloid. The probability that this BMP dimer will bind its receptors rather than another, yet uncleaved Chordin increases with the distance to the Chordin source (Fig. 1C). In Nematostella, the shuttling model was proposed when we found that, unlike in all bilaterian models studied thus far, depletion of Chordin results in the loss of BMP signaling rather than in its enhancement (34). However, given that, in Nematostella, BMP signaling indirectly represses the transcription of the core BMPs, BMP2/4 and BMP5-8, and activates the transcription of the modulator BMP, GDF5-like (14), an alternative explanation is also possible: In this “local inhibition” scenario, Chordin locally represses BMP signaling enabling BMP2/4 and BMP5-8 production. BMP2/4 and BMP5-8 diffuse into the area of low or no Chordin (i.e., to the GDF5-like side of the directive axis) and bind the receptors there. In this scenario, Chordin knockdown results in a transient de-repression of the BMP2/4/BMP5-8–mediated signaling, which, in turn, leads to the repression of the BMP2/4 and BMP5-8 transcription. Because, in the absence of BMP2/4 and BMP5-8, GDF5-like expression is also lost (9), we may end in a situation when no BMP ligands are produced and no BMP signaling takes place, as it is the case in the Chordin morphant (9, 34). This local inhibition model, in which Chordin acts exclusively as a local repressor of BMP signaling (Fig. 1D), is similar to the situation in zebrafish, where extracellular mobility of Chordin is not required (39–41). Here, we address the role of Chordin in the BMP-dependent axial patterning in the sea anemone Nematostella and test these two alternative models.

David Mörsdorf, Maria Mandela Prünster, Paul Knabl, Grigory Genikhovich.
Chordin-mediated BMP shuttling patterns the secondary body axis in a cnidarian.
Science Advances (2025) 11(24). DOI: 10.1126/sciadv.adu6347

Copyright: © 2025 The authors.
Published by the American Association for the Advancement of Science. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

This discovery poses a significant problem for creationist claims because it provides clear molecular and developmental evidence for a shared evolutionary origin between animals with bilateral symmetry and simpler organisms like sea anemones, which lack such symmetry as adults. The fact that the genetic and developmental mechanisms for establishing a "back" or body axis predate the emergence of bilaterally symmetrical animals suggests that these features evolved gradually through modification of existing biological systems—not through sudden, miraculous creation.

Creationism relies on the assertion that complex body plans appeared abruptly, fully formed, and without evolutionary precursors. However, the findings in this study directly contradict that idea. They show that the genetic toolkit required for bilateral body structures was already present in the common ancestor of cnidarians (like sea anemones) and bilaterians and was likely repurposed and elaborated upon over millions of years. This is exactly what evolutionary theory predicts.

Moreover, the study aligns neatly with the established evolutionary timeline based on genetics, developmental biology, and the fossil record. There is no need to invoke supernatural causes or to assume that animals were created independently and without shared ancestry. Instead, the evidence points to deep continuity in the genetic architecture of life—a hallmark of common descent and a major blow to the isolated, one-off acts of creation claimed by young-Earth and Intelligent Design creationists alike.

Malevolent Design - The Sneaky Way TB Keeps On Making Us Sick

Credit: Md Ariful Islam

Study discovers DNA switch that controls TB growth – and could help unlock its antibiotic resistance secrets | University of Surrey

If you're an omniscient, omnipotent, malevolent designer of parasites — such as the bacterium that causes tuberculosis in humans — then you're hardly going to let a little thing like the immune system (which you supposedly also designed to protect them) or even the development of medical science and antibiotics spoil your fun in causing random suffering, are you? Naturally, you'd equip your creation with mechanisms to overcome these obstacles.

Within the framework of Intelligent Design creationism, that's precisely what this recent discovery should look like — at least to those creationists who don't simply ignore the obvious and pretend it isn't there. Scientists from the Universities of Surrey and Oxford have discovered that Mycobacterium tuberculosis uses a reversible process known as ADP-ribosylation to modify its DNA, controlling both replication and gene expression. This allows the bacterium to remain dormant for extended periods and reactivate when environmental threats, such as immune responses or antibiotics, have passed.

This presents a problem for creationists who insist on believing in a benevolent creator deity and simultaneously hold that features such as irreducible complexity and complex specified information are sure signs of intelligent design—claims promoted by Discovery Institute fellows Michael J. Behe and William A. Dembski. Since Mycobacterium tuberculosis displays these very characteristics, so either it was designed specifically to cause suffering, or those characteristics are not the reliable indicators of divine design that Behe and Dembski claim, and their entire argument collapses.

This discovery was recently published open access in The EMBO Journal, and further details are available in the University of Surrey press release:

How Evolution Works - Co-opting Old Genes For New Functions

Liverworts lacking a gene called RLF have severe deformations in various organs (three plants pictured right and bottom), demonstrating that RLF is involved in organ development in these basic land plants as well.

© FUKAKI Hidehiro (CC BY)

Molecular phylogenetic tree of the REDUCED LATERAL ROOT FORMATION (RLF) protein family. The unrooted molecular phylogenetic tree was constructed based on amino acid sequences of RLF and CB5A, B, C, D, E, and LP from various plant species.

Iwata, K.P., Shimizu, T., Sakai, Y.,et al(2025)

A root development gene that’s older than root development | Kobe University News site

One common way creationist apologists attempt to mislead the scientifically uninformed is by claiming that the Laws of Thermodynamics are somehow relevant to the evolution of information within a species' genome. They argue that any increase in genetic information would violate both the Second and Third Laws of Thermodynamics—asserting that increased biological complexity equates to a decrease in entropy (disorder), and that new information is akin to energy and thus cannot increase due to the Law of Conservation.

This argument is fundamentally flawed on several levels but continues to be repeated despite being repeatedly refuted by both biologists and physicists. First, it completely ignores the fact that Earth is not a closed system. The input of energy from the Sun, for example, allows local decreases in entropy (such as in the formation of complex biological structures) while the total entropy of the universe still increases, fully complying with the Second Law. The Third Law, which relates to the entropy of systems at absolute zero, is entirely irrelevant to biological evolution.

Second, the idea that genetic information is conserved like energy is a misrepresentation. Genetic information can and does change in multiple ways through mutation. A mutation can involve the loss of information (e.g. deletion of a DNA segment), a change in information (e.g. substitution of one or more nucleotides), or an increase in information (e.g. insertion of additional sequences, or the movement of transposable elements—“jumping genes”—to new locations in the genome). None of these processes require a change in the total amount of matter or energy; they simply involve the rearrangement of existing molecular components. Any local increase in biological order is offset by energy expenditure elsewhere, typically via the hydrolysis of ATP to ADP and phosphate within metabolic pathways.

Moreover, these objections rest on the false assumption that evolution is about the quantity of information. In reality, it is the function and meaning of genetic information that drives evolutionary change. A sequence of DNA that once encoded a protein with one function can, through mutation and natural selection, take on a new function entirely—a process known as exaptation.

A well-known example is the evolution of the mammalian middle ear bones. In ancestral fish, certain jawbones played a structural role in the jaw joint. Over time, in early synapsids, these bones were repurposed and miniaturised to become part of the auditory system, transmitting sound vibrations from the eardrum to the cochlea.

Creationism Refuted - Evolution By Advantageous Mutation

This gene variant contributed to the dietary and physiological evolution of modern humans | ScienceDaily

One of the enduring claims in creationist circles is that mutations are invariably harmful—deleterious at best, fatal at worst—and thus incapable of driving evolutionary progress. This notion underpins Michael J. Behe's concept of "devolution," which posits that genetic changes represent a decline from an assumed state of original perfection. Yet, this perspective fails to account for how such "inferior" mutations could supplant their "perfect" predecessors in a population. Moreover, if a genome were truly perfect, it would replicate without error, precluding any mutations—and, by extension, any evolutionary change.

A recent study published in Cell Genomics challenges this dogma by identifying a regulatory variant of the ACSF3 gene that appears to have played a significant role in human evolution . This variant, known as rs34590044-A, enhances the expression of ACSF3 in the liver, influencing both stature and basal metabolic rate (BMR). Notably, the effects of this mutation are amplified in individuals consuming meat-rich diets, suggesting a link between genetic adaptation and dietary shifts in human history.[1.1,2.1]

The ACSF3 gene encodes an enzyme involved in mitochondrial fatty acid synthesis, a critical process for energy metabolism. Increased expression of ACSF3 has been associated with improved mitochondrial function and bone formation, potentially contributing to greater height and higher BMR in modern humans. These findings underscore the role of beneficial mutations in human adaptation and evolution, directly contradicting the creationist assertion that mutations cannot produce advantageous traits.[3.1,4.1]

This discovery not only provides insight into the genetic factors influencing human physiology but also exemplifies how mutations can facilitate evolutionary advancements, thereby challenging the notion that all genetic changes are inherently detrimental.

The team from Human Phenome Institute, Zhongshan Hospital and School of Life Sciences, Fudan University, Shanghai, China with Mark Stoneking, Department of Evolutionary Genetics, Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany, have recently published their findings in the open access Cell Press journal, Cell Genomics.

Creationism Refuted - How Mammalian Cold Adaptation Evolved - Starting 2.6 Million Years Before 'Creation Week'

Musk Ox, Ovibos moschatus

Arctic fox, Vulpes lagopus

Study reveals different phases of evolution during ice age | Bournemouth University

Creationists have yet another inconvenient science paper to ignore, misrepresent, or distort. A new study led by Professor John Stewart of Bournemouth University, UK, and published in Trends in Ecology & Evolution, presents compelling evidence that environmental change—specifically the climatic fluctuations of the Ice Age—has been a major driver of evolution.

By examining both fossil and palaeogenetic data in the context of glaciation records, the research team has shown that adaptations to cold climates began emerging around 2.6 million years ago. This evolutionary process significantly accelerated about 700,000 years ago, when glacial cycles shifted and cold periods began lasting twice as long. During warmer interglacial phases, cold-adapted species appear to have retreated into climatic refugia, only to expand again as the ice returned.

The main, but not the only, cause of these periods of alternating glaciation and warmer climate were the Milankovitch cycles. For details, see the AI information panel.

Reindeer, Rangifer tarandus

This study aligns closely with Darwinian evolutionary theory, and, contrary to claims by creationists that biologists are abandoning Darwinian evolution in favour of creationism, not with the metaphysical claims of intelligent design. Unsurprisingly, the researchers make no appeal to supernatural forces or pseudo-scientific conjecture. Instead, their work builds on and reinforces the evolutionary framework that has repeatedly proven its explanatory and predictive power.

Perhaps most damning to creationist dogma, the evolutionary events described took place hundreds of thousands—if not millions—of years before young-Earth creationists claim the planet was even formed. Depending on which apologetic is in play, creationists must now choose between proposing ludicrously accelerated post-Flood evolution or invoking the second law of thermodynamics in ways physicists and biologists would find baffling, using it to try to argue that events which can be observed could not have happened due to a fundamental law of physics.

Unintelligent Design - Bizarre Heath-Robinson Reproduction In A Marine Worm

[Body]

Close-up of female stolen – one of the independent reproductive units – from the worm Ramisyllis kingghidorahi. It has already sprouted eyes and is swimming free to find a stolon of the opposite sex with which to reproduce.

Information for the Media - Georg-August-Universität Göttingen

As a supposed product of intelligent design, the reproductive process of the branching marine worm Ramisyllis kingghidorahi is nothing short of bizarre—especially when one considers that many of its marine worm relatives manage perfectly well with far more straightforward, functional reproductive strategies, free from the Heath-Robinson complexity seen in R. kingghidorahi.

This remarkable worm comprises a branching network of segments, the ends of which can transform into free-living reproductive units known as stolons. These stolons firstly grow a pair of eyes then detach from the main body and swim off in search of a partner—another stolon of the opposite sex.

Yet the most pressing question for biologists isn’t why such a labyrinthine reproductive system evolved, but how it is controlled and coordinated across the worm’s sprawling body. This is precisely the mystery tackled by a team of researchers from Georg-August-Universität Göttingen, Germany.

Their research has just been published, open access, in the journal BMC Genomics.

Malevolent Designer News - How an Intelligent Designer COULD Have Made us all Immune to HIV but Chose not to

Researchers map 7,000-year-old genetic mutation that protects against HIV – University of Copenhagen

Let’s step into the mindset of an Intelligent Design (ID) creationist for a moment, as we examine a recent scientific study investigating why a small minority of people are immune to the Human Immunodeficiency Virus (HIV), while the vast majority are not.

A research team from the Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR) at the University of Copenhagen, led by Professor Simon Rasmussen, has discovered that this immunity is conferred by a genetic mutation. This mutation originated in a single individual who lived near the Black Sea between 6,700 and 9,000 years ago.

According to Discovery Institute Fellow William A. Dembski, this mutation would represent what he calls “complex specified information”, a concept he attributes to an intelligent designer. Dembski argues that only such a designer could create the necessary genetic information, as mutation and natural selection alone are not goal-directed and therefore cannot produce the desired specificity. However, Dembski is notably vague about how we can objectively determine what genetic information is “specified” and what is not. He appears to rely on subjective judgement, essentially deeming any beneficial mutation as “specified”, while dismissing deleterious mutations as irrelevant.

Even granting Dembski his biased subjectivity, we are left with the implication that the mutation which conferred HIV immunity to this individual's descendants must have been “specified” by his proposed intelligent designer.

This raises an obvious question: if the intelligent designer of humans could have provided our species with immunity to HIV, why did it choose not to do so from the outset? Why rely on what appears to be a slow, natural evolutionary process to spread this mutation through the population—one that depends on people dying of HIV while those with the mutation survive and reproduce, creating the selection pressure for its spread? A process so gradual that, to this day, it remains a rare trait in the human gene pool, with only 18-25% of Danes carrying the mutated gene.

It also raised a couple of theological question for creationists: why would an omnibenevolent creator create HIV with its 'designed' ability to bypass our immune system the same designer allegedly designed to protect us and how is that an intelligent act by an omnibenevolent deity?

Malevolent Design News - How An 'Irreducibly Complex' Jumping Gene Survives To Cause Cancer

Credit: Memorial Sloan Kettering Cancer Center.

Study Reveals Details of Process Driving Evolution & Major Diseases | NYU Langone News

A recent study by researchers at NYU Langone Health and Ludwig-Maximilians-Universität München has shed new light on how certain genetic elements, known as "jumping genes," contribute to both human evolution and the development of disease [1.1].

Intelligent Design (ID) proponents, such as Discovery Institute fellow William A. Dembski, claim that any genetic information which is both complex and specific can only originate from an intelligent designer. Similarly, Michael J. Behe argues that any complex biological structure or process requiring all its parts to function could not have evolved gradually and therefore must have been deliberately designed.

These arguments rest on little more than the fallacies of argument from incredulity and the God-of-the-gaps. Worse still, they inevitably raise troubling theological implications: if such "complex specified information" leads to harmful outcomes—such as diseases, congenital disorders, or parasitism—then their supposed designer must be incompetent, indifferent, or malevolent. In the case at hand, the study focuses on a type of "jumping gene," or retrotransposon, which is known to cause genetic diseases including cancers.

Proponents of ID consistently sidestep these issues, as they conflict with their effort to portray the Bible as a scientifically accurate text describing a benevolent, human-centred creator.

Malevolent Design - How Dembski's 'Complex Specified Information' Causes Acute Myeloid Leukemia

Rapid growth of blood cancer driven by a single genetic ‘hit’

William A. Dembski’s concept of complex specified information (CSI) remains ambiguous—arguably by design. His use of the word specified is particularly opaque: is he referring to information that produces outcomes he wishes his readers to believe are purposeful and intelligently designed by a particular deity, or is the term intended to encompass any genetic information that results in any outcome—beneficial, neutral, or harmful?

Taken at face value, and in the absence of a clear, testable definition, there appears to be no reason Dembski’s concept could not apply to information that is ultimately detrimental, either to the organism itself, or to another organism in the case of parasites or cancer. Why, for instance, should we conclude that the complex information in a gene enabling the expansion of the human brain and the enhancement of cognitive function was specified, but that the equally complex genetic information enabling a cell to become a malignant cancer, or allowing the Plasmodium falciparum parasite to evade anti-malarial drugs, was not also specified by the same intelligent designer?

Given that Dembski is a senior fellow of the Discovery Institute — an organisation notorious for its Wedge Strategy, which seeks to undermine public trust in science through disinformation and misrepresentation while promoting creationism under the guise of scientific legitimacy — it is unsurprising that complex specified information remains a nebulous and ill-defined term. The strategy’s aim has never been to engage in genuine scientific discourse or subject its claims to critical scrutiny, but rather to advance a religious agenda while avoiding the accountability that comes with reasoned analysis and empirical testing. A cynic might conclude that the leading ID advocates know their claim has no scientific basis but want their target audience to believe otherwise.

So, I invite Intelligent Design creationists to explain why the recent discovery of a gene that promotes the rapid early development of acute myeloid leukaemia should not be an example of Dembski's 'complex specified information' and so evidence that Dembski's intelligent designer designed acute myeloid leukaemia, or whether Dembski's term is deliberately vague so as to appeal to people looking for confirmation of existing bias.

Unintelligent Design - If Scientists Can Do It, Why Can't an Intelligent, Omnipotent Designer - If It Wanted To?

Treatment for mitochondrial diseases within reach | University of Gothenburg

If the human body had truly been intelligently designed by an omnibenevolent, omniscient deity, it would operate flawlessly under all conditions, free from the compromises and constraints inherent in evolutionary history.

Were this the case, much of modern medicine would be unnecessary, limited perhaps to the management and repair of traumatic injuries. Parasites, should they exist at all, would be effortlessly repelled by a perfect immune system. Genetic and structural defects, such as hernias, atherosclerosis, autoimmune disorders, blindness, deafness, neurodegenerative diseases, and complications in childbirth would simply not occur.

However, as I showed in my book, The Body of Evidence: How the Human Body Refutes Intelligent Design, the human body is not the product of intelligent design; it has evolved through a process marked by trial and error, adaptation to existing structures, and the utilitarian pressures of survival and reproduction. This explains the vast array of medical conditions that keep healthcare systems busy, often stretched to their limits. It also drives the extensive scientific research dedicated to discovering the causes and developing cures for various illnesses—achievements that an omnipotent and omnibenevolent creator, if one existed, presumably would have provided already.

Recent news highlights this contrast starkly. Scientists may have discovered a groundbreaking cure for a rare mitochondrial disease caused by mutations in the POLG gene, a condition that leads to severe disability or even early death. This advancement prompts a critical question for creationists: If human scientists can find solutions to such devastating genetic problems, why can't—or won't—your purported intelligent designer? And perhaps, more to the point, why was this defect designed in the first place?

Unintelligent Design - Another Failure By Creationism's Blundering Designer

Machine for repairing broken mtDNA.

AI-Generated image
(with apologies to William Heath Robinson)

The graphic shows images of a cell under mtDNA replication stress made using so-called Correlative Light and Electron Microscopy (for short: CLEM). The mitochondrial DNA (mtDNA, green) is ejected from the mitochondria (magenta) and taken up by a lysosome, which contains the retromer (cyan). The highlighted section was also analysed using 3D-CLEM to obtain volumetric information.

Fig.: HHU/David Pla-Martín.

Medicine: Publication in Science Advances

Yet Another Workaround for a Flawed Design.

Researchers led by Professor Dr David Pla-Martín of Heinrich Heine University Düsseldorf, alongside colleagues from the University of Cologne, have uncovered yet another complex but error-prone workaround—this time, to fix a problem that stems from an earlier design flaw.

They have identified a mechanism used to repair mitochondrial DNA (mtDNA) when it breaks. From an intelligent design perspective, mitochondria — once free-living bacteria—were supposedly the 'quick fix' to give eukaryotic cells the ability to efficiently convert glucose into adenosine triphosphate (ATP) using oxygen. ATP is the primary energy currency used in metabolic reactions, formed from adenosine diphosphate (ADP) and phosphate.

A truly intelligent designer, however, could have simply endowed cells with this biochemical machinery from the start—no need to incorporate foreign bacteria complete with their own DNA. But apparently, that would have been too simple.

This convoluted solution, predictably, comes with problems. Mitochondria often replicate their DNA imperfectly, or the DNA becomes damaged, leading to mitochondrial failure and a range of diseases. So, yet another layer of biological complexity has evolved to patch up the broken mtDNA. And, in classic Heath Robinson fashion, this repair mechanism is itself error-prone.

Refuting Creationsm - Evolution By Loss of Genes, Horizontal Gene Transfer And Gene Duplication

Nitzschia sp

By Kristian Peters - Own work,
CC BY-SA 3.0,
Wikimedia

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Nitzschia sing1 lives on the alginate in the cell walls of decaying brown algae.

A borrowed bacterial gene allowed some marine diatoms to live on a seaweed diet | PRESS-NEWS.org

A fundamental axiom of creationism is the claim that any loss of genetic information is invariably detrimental—so much so that any mutation resulting in such a loss would be fatal and could therefore play no role in evolution. A second axiom asserts that new genetic information cannot arise naturally and must instead be supplied by a supernatural intelligent designer.

Both of these assertions are demonstrably false. Nevertheless, they continue to feature in creationist apologetics, relying on the audience's ignorance and incredulity to pass as justification for belief in an intelligent creator.

To add further difficulty for creationist claims, scientists have now identified a marine diatom, Nitzschia sing1, that has not only lost the genes and organelles required for photosynthesis — present in its photosynthetic relatives — but has also adapted successfully without them. It achieved this by acquiring new genetic information through horizontal gene transfer from a marine bacterium. The transferred gene subsequently underwent extensive duplication and diversification into three gene families, each with complementary functions. Together, these 91 versions of the acquired gene enable N. sing1 to metabolise alginate, a carbohydrate found in the cell walls of brown algae such as kelp.