Rosa Rubicondior: Malevolent Designer - We COULD Have Been Designed To Resist Snake Venom

Major Skink, Bellatorias frerei

How Aussie skinks outsmart lethal snake venom - News - The University of Queensland

As though the recent news from the biological sciences wasn't already bad enough for creationists, we now have two examples demonstrating how—if an omnibenevolent, omniscient deity really had designed humans as the pinnacle of creation—it could have done a far better job. Yet, apparently, it chose not to.

The first, which is the subject of this blog post, involves a seemingly humble Australian lizard, the major skink (Bellatorias frerei), which possesses a simple mutation that renders it immune to Australian snake venom.

The second example, which I’ll cover in my next post, concerns the apple snail. This remarkable mollusc has an eye that is structurally and genetically similar to the mammalian eye—but unlike ours, it can regenerate if damaged or lost. But more on that later.

Australia is infamous for its venomous snakes—many of them deadly. Yet thanks to the widespread availability of antivenoms, there are only one or two fatalities annually, out of hundreds of snakebite cases.

However, if humans had been endowed with the same mutation as the skink, there would be no deaths at all—and no need for antivenoms. Interestingly, this is the same mutation that grants immunity to cobra venom in some mammals, such as mongooses and honey badgers. So, from a creationist perspective, there appears to be no good reason to deprive humans of this mutation — unless the designer was malevolent, indifferent, or just lazy.

It would pose an interesting challenge to intelligent design (ID) creationists to explain the "intelligence" in designing snakes to kill lizards with neurotoxic venom, only to then design lizards that are immune to it. Of course, creationists invariably avoid addressing these sorts of paradoxes—paradoxes which evolutionary biology easily explains as the outcome of an unintelligent evolutionary arms race.

These neurotoxic venoms work by binding to receptors on the surface of muscle cells and blocking the action of the neurotransmitter acetylcholine. This prevents muscle contraction, ultimately stopping respiration. The simple mutation in the skinks alters these receptors so that the venom can no longer bind effectively, neutralising its effects.

The Evolution and Origins of Australia’s Elapid Snakes. Australia is home to some of the world’s most venomous snakes, including taipans, brown snakes, and tiger snakes. All of these belong to a single family: Elapidae, a group of front-fanged venomous snakes also found in Africa, Asia, and the Americas. However, what sets Australia’s elapids apart is their extraordinary diversity — over 100 species — and their evolutionary origins, which trace back to an unexpected source: the sea.

Marine Origins

A 2022 study led by researchers from the University of Adelaide has shed new light on how these iconic snakes came to be. By analysing the genomes of elapid snakes from around the world, the team concluded that all Australian terrestrial elapids descended from a single marine ancestor, likely a type of sea snake that arrived in Australia roughly 25 million years ago during the late Oligocene to early Miocene.

At that time, Australia was geographically isolated and largely devoid of advanced land snakes. When this marine ancestor arrived—possibly via ocean currents from Asia or the Indo-Pacific—it found a continent rich in potential prey but with few competitors. This set the stage for a remarkable adaptive radiation, giving rise to the wide variety of elapid species seen in Australia today, from the inland taipan (the world’s most venomous snake) to small burrowing forms like the vermiculate snake.

Jumping Genes from the Sea

One of the study’s most intriguing findings involves horizontal gene transfer — the acquisition of DNA from unrelated species, a phenomenon previously thought to be rare in vertebrates. The researchers found evidence of so-called “jumping genes” (transposable elements) in the genomes of Australian elapids that are nearly identical to those found in marine organisms such as fish and tunicates.

This suggests that *during their marine phase, these ancestral snakes acquired genes from other sea-dwelling organisms—possibly through parasitic vectors like marine worms or viruses. These genes may have played a role in the snakes’ rapid adaptation to new environments once they came ashore, although the exact function of the transferred sequences remains under investigation.

Adaptive Radiation on Land

Once established on land, Australian elapids diversified rapidly. With little initial competition and abundant ecological niches to fill, they evolved into an astonishing array of forms. Some remained highly venomous ambush predators, while others adapted to fossorial (burrowing) or even arboreal lifestyles. Natural selection, driven by prey availability, climate, and predator-prey arms races, sculpted this radiation.

Today, all native Australian land snakes are elapids. There are no native vipers or colubrids with a strong ecological presence, as seen on other continents — another testament to the evolutionary head start this single marine ancestor provided.

The team that made this discovery, led by Professor Bryan Fry from the University of Queensland’s School of the Environment, also found that the same mutation had independently arisen at least 25 separate times in Australian skinks. This occurred in the ~20 million years since the arrival of venomous elapid snakes—such as taipans—on the continent. These snakes, likely descended from a marine ancestor, would have found a plentiful supply of naïve prey species, exerting intense selection pressure on the lizards to evolve resistance.

The team’s findings are published open access in the International Journal of Molecular Sciences. A summary is also provided in a University of Queensland news release.

How Aussie skinks outsmart lethal snake venom
Key points

UQ researchers found 25 independent instances of neurotoxin resistance in Australian skinks.
The resistance evolved after poisonous elapid snakes such as taipans arrived in Australia.
Understanding how skinks dodge death provides insights for future biomedical approaches to treating snakebite.

A University of Queensland-led study has found Australian skinks have evolved molecular armour to stop snake venom from shutting down their muscles.

Professor Bryan Fry from UQ’s School of the Environment said revealing exactly how skinks dodge death could inform biomedical approaches to treating snakebite in people.

What we saw in skinks was evolution at its most ingenious. Australian skinks have evolved tiny changes in a critical muscle receptor, called the nicotinic acetylcholine receptor. This receptor is normally the target of neurotoxins which bind to it and block nerve-muscle communication causing rapid paralysis and death. But in a stunning example of a natural counterpunch, we found that on 25 occasions skinks independently developed mutations at that binding site to block venom from attaching. It’s a testament to the massive evolutionary pressure than venomous snakes exerted after their arrival and spread across the Australian continent, when they would have feasted on the defenceless lizards of the day. Incredibly, the same mutations evolved in other animals like mongooses which feed on cobras. We confirmed with our functional testing that Australia’s Major Skink (Bellatorias frerei) has evolved exactly the same resistance mutation that gives the honey badger it’s famous resistance to cobra venom. To see this same type of resistance evolve in a lizard and a mammal is quite remarkable – evolution keeps hitting the same molecular bullseye.

Professor Bryan G. Fry, corresponding author.
Adaptive Biotoxicology Lab
School of the Environment
University of Queensland, St Lucia, QLD, Australia.

The muscle receptor mutations in the skinks included a mechanism to add sugar molecules to physically block toxins and the substitution of a protein building block (amino acid arginine at position 187).

The laboratory work validating the mutations was carried out at UQ’s Adaptive Biotoxicology Laboratory by Dr Uthpala Chandrasekara who said it was incredible to witness.

We used synthetic peptides and receptor models to mimic what happens when venom enters an animal at the molecular level and the data was crystal clear, some of the modified receptors simply didn’t respond at all. It’s fascinating to think that one tiny change in a protein can mean the difference between life and death when facing a highly venomous predator.

Dr. Uthpala Chandrasekara, first author
Adaptive Biotoxicology Lab
School of the Environment
University of Queensland, St Lucia, QLD, Australia.

The findings could one day inform the development of novel antivenoms or therapeutic agents to counter neurotoxic venoms.

Understanding how nature neutralises venom can offer clues for biomedical innovation. The more we learn about how venom resistance works in nature, the more tools we have for the design of novel antivenoms.

Dr. Uthpala Chandrasekara.

The project included collaborations with museums across Australia.

Publication:
Chandrasekara, U.; Mancuso, M.; Shea, G.; Jones, L.; Kwiatkowski, J.; Trembath, D.; Chowdhury, A.; Bertozzi, T.; Gardner, M.G.; Hoskin, C.J.; et al.
Make Acetylcholine Great Again! Australian Skinks Evolved Multiple Neurotoxin-Proof Nicotinic Acetylcholine Receptors in Defiance of Snake Venom. Int. J. Mol. Sci. 2025, 26, 7510. https://doi.org/10.3390/ijms26157510.

Abstract
Many vertebrates have evolved resistance to snake venom as a result of coevolutionary chemical arms races. In Australian skinks (family Scincidae), who often encounter venomous elapid snakes, the frequency, diversity, and molecular basis of venom resistance have been unexplored. This study investigated the evolution of neurotoxin resistance in Australian skinks, focusing on mutations in the muscle nicotinic acetylcholine receptor (nAChR) α1 subunit’s orthosteric site that prevent pathophysiological binding by α-neurotoxins. We sampled a broad taxonomic range of Australian skinks and sequenced the nAChR α1 subunit gene. Key resistance-conferring mutations at the toxin-binding site (N-glycosylation motifs, proline substitutions, arginine insertions, changes in the electrochemical state of the receptor, and novel cysteines) were identified and mapped onto the skink organismal phylogeny. Comparisons with other venom-resistant taxa (amphibians, mammals, and reptiles) were performed, and structural modelling and binding assays were used to evaluate the impact of these mutations. Multiple independent origins of α-neurotoxin resistance were found across diverse skink lineages. Thirteen lineages evolved at least one resistance motif and twelve additional motifs evolved within these lineages, for a total of twenty-five times of α-neurotoxic venoms resistance. These changes sterically or electrostatically inhibit neurotoxin binding. Convergent mutations at the orthosteric site include the introduction of N-linked glycosylation sites previously known from animals as diverse as cobras and mongooses. However, an arginine (R) substitution at position 187 was also shown to have evolved on multiple occasions in Australian skinks, a modification previously shown to be responsible for the Honey Badger’s iconic resistance to cobra venom. Functional testing confirmed this mode of resistance in skinks. Our findings reveal that venom resistance has evolved extensively and convergently in Australian skinks through repeated molecular adaptations of the nAChR in response to the enormous selection pressure exerted by elapid snakes subsequent to their arrival and continent-wide dispersal in Australia. These toxicological findings highlight a remarkable example of convergent evolution across vertebrates and provide insight into the adaptive significance of toxin resistance in snake–lizard ecological interactions.

Graphical Abstract

Chandrasekara, U.; Mancuso, M.; Shea, G.; Jones, L.; Kwiatkowski, J.; Trembath, D.; Chowdhury, A.; Bertozzi, T.; Gardner, M.G.; Hoskin, C.J.; et al.
Make Acetylcholine Great Again! Australian Skinks Evolved Multiple Neurotoxin-Proof Nicotinic Acetylcholine Receptors in Defiance of Snake Venom. Int. J. Mol. Sci. 2025, 26, 7510. https://doi.org/10.3390/ijms26157510.

Copyright: © 2025 The authors.
Published by MDPI (Basel, Switzerland). Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

Why This Matters — and Why It's a Problem for Creationism.

The discovery that Australian skinks have independently evolved resistance to snake venom on at least 25 occasions offers yet another clear example of natural selection in action. It demonstrates how evolutionary arms races between predator and prey drive adaptive changes over time, with no need for foresight, planning, or intelligent design. A simple mutation, providing a survival advantage, is favoured and passed on—entirely consistent with Darwinian evolution.

For creationists, however, this presents an awkward dilemma. If humans were intentionally designed by an all-powerful, all-knowing, and benevolent creator, why weren’t we given the same mutation that protects skinks, mongooses, and honey badgers from neurotoxic venom? Why must we rely on medical interventions like antivenoms—developed through painstaking scientific effort—rather than benefit from a built-in biological defence?

Even more troubling for Intelligent Design proponents is the broader ecological narrative: venomous snakes evolved to kill prey; prey evolved resistance to venom. The logic of such a system defies any notion of benevolence or intelligent planning. It looks exactly as we’d expect under a model of unguided, evolutionary trial and error.

Put simply, evolution explains these patterns elegantly. Creationism doesn’t explain them at all.

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