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Nature’s Armor: Scientists Uncover Gene Behind Aussie Skinks’ Immunity to Deadly Snake Venom

In a groundbreaking study led by the University of Queensland, scientists have discovered the genetic secret behind Australian skinks’ remarkable ability to withstand deadly snake venom. The research, published in the International Journal of Molecular Sciences, reveals that these small lizards have evolved a molecular armor to protect themselves from the toxic effects of neurotoxins.

Professor Bryan Fry from UQ’s School of the Environment explained that the skinks’ defense mechanism involves tiny changes in a critical muscle receptor called the nicotinic acetylcholine receptor. This receptor is normally targeted by snake venom, which blocks nerve-muscle communication and leads to rapid paralysis and death. However, in a stunning example of evolutionary adaptation, researchers found that skinks independently developed mutations on 25 occasions to block venom from attaching.

“It’s a testament to the massive evolutionary pressure exerted by venomous snakes after their arrival and spread across the Australian continent,” Professor Fry said. “The same mutations evolved in other animals like mongooses, which feed on cobras.”

Researchers confirmed that Australia’s Major Skink (Bellatorias frerei) has developed exactly the same resistance mutation as the honey badger, famous for its immunity to cobra venom.

To validate these findings, scientists conducted functional testing at UQ’s Adaptive Biotoxicology Laboratory. Dr. Uthpala Chandrasekara led the laboratory work and reported that the data was “crystal clear.” The modified receptors simply didn’t respond to toxins, demonstrating their remarkable ability to repel deadly snake venom.

This research has significant implications for biomedical innovation, particularly in the development of novel antivenoms or therapeutic agents. Dr. Chandrasekara emphasized that understanding how nature neutralizes venom can provide valuable clues for designing more effective treatments.

The project involved collaborations with museums across Australia and offers a promising example of interdisciplinary research, bridging the gap between scientific discovery and potential applications.

The article “Unlocking the Gut-Brain Connection: Scientists Discover Hidden ‘Neurobiotic Sense’ that Talks to Your Brain” reveals a groundbreaking discovery in the field of neuroscience. Researchers at Duke University School of Medicine have uncovered a previously unknown system, dubbed the “neurobiotic sense,” which enables the brain to respond rapidly to signals from microbes living in the gut.

The study, led by Diego Bohórquez, PhD, and M. Maya Kaelberer, PhD, centers on neuropods – tiny sensor cells lining the colon’s epithelium. These cells detect a common microbial protein called flagellin, which is released by some gut bacteria when we eat. The neuropods then send rapid messages to the brain through the vagus nerve, helping curb appetite.

The researchers propose that this neurobiotic sense may be a broader platform for understanding how the gut detects microbes, influencing everything from eating habits to mood and even how the brain might shape the microbiome in return. This could have significant implications for conditions like obesity or psychiatric disorders.

The team tested their hypothesis by fasting mice overnight and then giving them a small dose of flagellin directly to the colon. The mice that received flagellin ate less, while those missing the TLR5 receptor (a crucial component of the pathway) continued to eat and gained weight. This suggests that flagellin sends a “we’ve had enough” signal through TLR5, allowing the gut to tell the brain it’s time to stop eating.

The discovery was guided by lead study authors Winston Liu, MD, PhD, Emily Alway, both graduate students of the Medical Scientist Training Program, and postdoctoral fellow Naama Reicher, Ph.D. Their experiments reveal that disrupting the pathway altered eating habits in mice pointed to a deeper link between gut microbes and behavior.

As Bohórquez notes, this work will be especially helpful for the broader scientific community to explain how our behavior is influenced by microbes. A clear next step is to investigate how specific diets change the microbial landscape in the gut – a key piece of the puzzle in conditions like obesity or psychiatric disorders.

The battle against cancer has long been an uphill struggle. Despite advances in treatment, the disease still claims too many lives. However, scientists have made a groundbreaking discovery that could change the game – starving tumors to make cancer treatment more effective.

Cancer cells and tumors do not exist in isolation. They interact with their surrounding environment, which is composed of immune cells, connective tissue, blood vessels, and proteins and carbohydrates that provide structure and other supportive functions. Pancreatic ductal adenocarcinoma (PDAC) cells, for instance, use a cellular scavenging process called macropinocytosis to grab extra nutrients from the extracellular matrix.

Macropinocytosis affects the area surrounding the tumor, making connective tissue stiffer and preventing immune cells from reaching the tumor. Researchers at the NCI-Designated Cancer Center at Sanford Burnham Prebys published findings in Cancer Cell demonstrating that blocking macropinocytosis reshapes the tumor microenvironment to be less fibrous and allows more access to immune cells.

The researchers observed that nearby fibroblasts, which typically form connective tissue and produce many components of the extracellular matrix captured during macropinocytosis, are coerced to become cancer-associated fibroblasts (CAF) that help tumors grow. These CAFs provide metabolites and growth signals, as well as helping in other ways.

When macropinocytosis was blocked, CAFs experienced metabolic stress due to deprivation of glutamine, one of the 20 amino acids used to build proteins throughout the body. PDAC relies heavily on glutamine, so CAFs in the pancreatic cancer tumor microenvironment are regularly starved of it.

Preventing macropinocytosis led to a change to a different subtype of CAF marked by the expression of genes that promote inflammation. This altered CAF population had fewer myofibroblasts, which make the tumor microenvironment stiff and fibrotic, and more inflammatory CAFs, which allow for greater access to immune cells.

The research team found significant changes in the tumor neighborhood resulting from preventing macropinocytosis in CAFs. There were fewer deposits of collagen that make the tumor microenvironment stiff or fibrotic, more access for CD4+ and CD8+ T cells to infiltrate the tumor, and vascular expansion, which promotes drug delivery.

The investigators then tested the effects of combining a treatment to block macropinocytosis with immunotherapy and chemotherapy. They found that this combination significantly suppressed tumor metastasis and prolonged mouse survival.

These findings have significant implications for cancer patients, particularly those with PDAC, which is the third leading cause of cancer deaths despite accounting for only three percent of cases. The scientists will continue to explore how to prevent tumors from scavenging energy to reshape the tumor microenvironment into one that makes cancer treatments more effective.

As lead author Yijuan Zhang, PhD, said, “We believe this is a very promising strategy to pursue for developing combination therapies for cancer patients.”