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Biology

The Hidden Parasites of Our DNA: Uncovering the Role of Introners in Genetic Complexity

A new study proves that a type of genetic element called ‘introners’ are the mechanism by which many introns spread within and between species, also providing evidence of eight instances in which introners have transferred between unrelated species in a process called ‘horizontal gene transfer,’ the first proven examples of this phenomenon.

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The genetic code that governs every living organism is not always beneficial. Some parts of DNA act like parasites, relying on the host for survival while contributing little to its overall well-being. These “selfish” genes are called introners, and they have been found to play a significant role in the evolution of genetic complexity.

Researchers from the University of California, Santa Cruz, have conducted a study that proves introners are responsible for many of these selfish genes spreading within and between species. This discovery sheds light on how genomes evolved to become so complex and could potentially be leveraged in human health research.

Introners are non-coding DNA segments that must be removed before proteins can be produced. They have been found to exist in varying amounts across all animals, plants, fungi, and protists, and have managed to successfully replicate themselves and survive despite not serving an evolutionary function.

The researchers, led by Russ Corbett-Detig, senior author on the study and professor of biomolecular engineering at the Baskin School of Engineering, have spent years studying introns. They wanted to understand why these non-protein-coding bits of DNA are seen in different amounts across species and how they have managed to replicate themselves.

Their research has shown that introners are a type of transposable element, also known as “jumping genes,” that can move from one part of the genome to another. They have found evidence for 1,093 families of introners among the 8,716 genomes analyzed, suggesting that there are many kinds of introners capable of spreading introns through the genomes of various species.

One of the most significant findings of this study is the first direct evidence for horizontal gene transfer of introners. The researchers found eight examples of an introner hopping out of the genome of one species and settling into the genome of another unrelated species that mating could not explain. This phenomenon has been observed in species as diverse as sea sponges, marine protists, and fungi.

The researchers propose that introners may be hitchhiking on giant viruses to transfer between species. This would mean that these selfish genetic elements are using other selfish elements to spread themselves throughout the genome.

While this study provides valuable insights into the evolution of genetic complexity, it also highlights the potential risks associated with introners. The process of alternative splicing, which is crucial for creating different versions of proteins from a single gene, can lead to health problems if it breaks a gene. Many researchers are studying how alternative splicing can be studied to better understand genetic disease.

In conclusion, the discovery of introners and their role in spreading selfish genes within and between species has significant implications for our understanding of genome evolution and human health research. Further studies on these hidden parasites of our DNA could potentially lead to breakthroughs in the treatment of genetic diseases.

Animals

Sugar-Based Sensors Revolutionize Snake Venom Detection

Researchers have published the first example of a synthetic sugar detection test for snake venom, offering a new route to rapid diagnosis and better antivenoms.

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The detection of snake venom is a crucial step in treating life-threatening snake bites. According to the World Health Organization (WHO), every five minutes, 50 people are bitten by a snake worldwide, resulting in four permanent disabilities and one death. Traditional methods for diagnosing snake venom rely on antibodies, which have limitations such as high costs, lengthy procedures, and inconsistencies.

Researchers at the University of Warwick have made a groundbreaking discovery that could revolutionize snake venom detection. They have developed a glycopolymer-based ultraviolet-visible (UV-vis) test to detect Western Diamondback Rattlesnake (Crotalus atrox) venom. This new assay is a cheap and rapid alternative to antibody-based approaches, showcasing a version that specifically detects Crotalus atrox venom.

Dr. Alex Baker, lead researcher of the Baker Humanitarian Chemistry Group, explained that snake venoms are complex, making it challenging to detect toxins in the body. However, their research has produced an assay using synthetic sugars that mimic the natural sugar receptors targeted by venom proteins. The team engineered synthetic chains of sugar-like units (glycopolymers) attached to gold nanoparticles to amplify the response and make the reaction visible.

The Western Diamondback Rattlesnake venom binds to specific sugar molecules on red blood cells and platelets, disrupting blood clotting or interfering with immune responses leading to disability and death. The new assay changes color when venom toxins bind to the synthetic sugars, providing a rapid and cheap detection method beyond antibody-based techniques.

Mahdi Hezwani, first author of the research paper, emphasized that this assay could be a game-changer for snake envenomation. The team tested venom from other snake species, such as the Indian Cobra (Naja naja), and found that it did not interact with glycans in the body. This suggests that the new assay may have potential to distinguish between different snake venoms based on their sugar-binding properties.

This is the first example of a diagnosis test using sugars for detecting snake venom in a rapid detection system, building on the work of the Warwick research group using a glyconanoparticle platform in COVID-19 detection. The new assay is faster, cheaper, and easier to store, making it a more practical solution for treating snake bites.

The University of Warwick’s STEM Connect programme has enabled this innovative research, demonstrating the potential for bold and innovative solutions in addressing global health challenges.

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Animal Learning and Intelligence

The Buzz on Caffeine: How it Affects the Sleeping Brain

Coffee can help you stay awake. But what does caffeine actually do to your brain once you’re asleep? Using AI, a team of researchers has an answer: it affects the brain’s ‘criticality’.

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The article delves into the intricate relationship between caffeine and the sleeping brain, offering fresh insights from a recent study published in Nature Communications Biology. Researchers from Université de Montréal have shed new light on how caffeine can modify sleep patterns and influence the brain’s recovery during the night.

Led by Philipp Thölke, a research trainee at UdeM’s Cognitive and Computational Neuroscience Laboratory (CoCo Lab), the team used AI and electroencephalography (EEG) to study caffeine’s effects on sleep. Their findings reveal that caffeine increases the complexity of brain signals and enhances brain “criticality” during sleep – a state characterized by balanced order and chaos.

Interestingly, this effect is more pronounced in younger adults, particularly during REM sleep, the phase associated with dreaming. The researchers attribute this finding to a higher density of adenosine receptors in young brains, which naturally decrease with age. Adenosine is a molecule that accumulates throughout the day, causing fatigue.

The study’s lead author, Thölke, notes that caffeine stimulates the brain and pushes it into a state of criticality, where it is more awake, alert, and reactive. However, this state can interfere with rest at night, preventing the brain from relaxing or recovering properly.

The researchers used EEG to record the nocturnal brain activity of 40 healthy adults on two separate nights: one when they consumed caffeine capsules three hours before bedtime and another when they took a placebo at the same time. They applied advanced statistical analysis and artificial intelligence to identify subtle changes in neuronal activity, revealing that caffeine increased the complexity of brain signals during sleep.

The team also discovered striking changes in the brain’s electrical rhythms during sleep: caffeine attenuated slower oscillations such as theta and alpha waves – generally associated with deep, restorative sleep – and stimulated beta wave activity, which is more common during wakefulness and mental engagement.

These findings suggest that even during sleep, the brain remains in a more activated, less restorative state under the influence of caffeine. This change in the brain’s rhythmic activity may help explain why caffeine affects the efficiency with which the brain recovers during the night, with potential consequences for memory processing.

The study’s implications are significant, particularly given the widespread use of caffeine as a daily remedy for fatigue. The researchers stress the importance of understanding its complex effects on brain activity across different age groups and health conditions. They add that further research is needed to clarify how these neural changes affect cognitive health and daily functioning, potentially guiding personalized recommendations for caffeine intake.

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Biology

Unraveling Microtubule Mysteries: Scientists Crack Code on Cellular Scaffolding Secrets

Scientists found out how naturally unstable filaments decide whether to grow or to shorten.

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A groundbreaking study has shed new light on the fundamental mechanisms governing microtubule growth within cells. Researchers from Queen Mary University of London and the University of Dundee have made a significant breakthrough by discovering that the ability of tubulin proteins at microtubule ends to connect with each other sideways determines whether a microtubule elongates or shortens.

Microtubules are crucial protein structures that form the internal skeleton of cells, providing structural support and generating dynamic forces that push and pull. These tiny filaments constantly assemble and disassemble by adding or removing tubulin building blocks at their ends. However, the precise rules dictating whether a microtubule grows or shrinks have long remained a mystery due to the complexity and miniature size of their ends.

The collaborative research team has cracked part of this code using advanced computer simulations coupled with innovative imaging techniques. This interdisciplinary approach has allowed them to address this complex biological question from a fresh perspective, bridging physics and biology.

Dr. Vladimir Volkov, co-lead author from Queen Mary University of London, explained the significance of their findings: “Understanding how microtubules grow and shorten is very important – this mechanism underlies division and motility of all our cells. Our results will inform future biomedical research, particularly in areas related to cell growth and cancer.”

Dr. Maxim Igaev, co-lead author from the University of Dundee, highlighted the power of their interdisciplinary approach: “Bridging physics and biology has allowed us to address this complex biological question from a fresh perspective. This synergy not only enriches both fields but also paves the way for discoveries that neither discipline could achieve in isolation.”

This exciting research deepens our understanding of fundamental cellular processes and opens potential new avenues for biomedical research, particularly in areas concerning cell proliferation and the development of treatments for diseases like cancer.

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