澳大利亚石龙子通过突变关键肌肉受体，形成了抵抗毒蛇咬伤的非凡基因防御机制，使其对神经毒素产生抵抗力。这些微小但强大的分子变化与猫鼬、蜜獾等抗眼镜蛇毒哺乳动物的变异特征高度一致。这场进化军备竞赛不仅展现了生命的强大适应性，更为人类医学领域创造新型抗蛇毒血清和疗法提供了激动人心的可能性。
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," Professor Fry said.
"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 defenseless 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."
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," said Dr Chandrasekara.
"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."
The findings could one day inform the development of novel antivenoms or therapeutic agents to counter neurotoxic venoms.
"Understanding how nature neutralizes venom can offer clues for biomedical innovation," Dr Chandrasekara said.
"The more we learn about how venom resistance works in nature, the more tools we have for the design of novel antivenoms."
The project included collaborations with museums across Australia.
The research has been published in International Journal of Molecular Sciences.