Researchers decipher mechanism that prevents the loss of brown adipose tissue activity during ageing

From left to right, Tania Quesada-López, Francesc Villarroya, Albert Blasco-Roset, Marta Giralt, Alberto Mestres-Arenas, Joan Villarroya, Aleix Gavaldà-Navarro and Rubén Cereijo.
Photo Credit: Courtesy of University of Barcelona

As the body ages, brown adipose tissue activity decreases, fewer calories are burned, and this can contribute to obesity and certain chronic cardiovascular diseases that worsen with age. A study led by the University of Barcelona has identified a key molecular mechanism in the loss of brown fat activity during ageing. The study opens up new perspectives for designing strategies to boost the activity of this tissue and prevent chronic metabolic and cardiovascular diseases as the population ages.

The paper, published in the journal Science Advances, is led by Professor Joan Villarroya, from the Faculty of Biology and the Institute of Biomedicine of the UB (IBUB) — based at the Barcelona Science Park-UB  — and the CIBER Area for Physiopathology of Obesity and Nutrition  (CIBEROBN). Teams from the Albert Einstein College of Medicine in New York (United States) are also collaborating.

UQ scientists uncover secrets of yellow fever

Dr Summa Bibby
Photo Credit: The University of Queensland

University of Queensland researchers have captured the first high-resolution images of the yellow fever virus (YFV), a potentially deadly viral disease transmitted by mosquitoes that affects the liver.

They’ve revealed structural differences between the vaccine strain (YFV-17D) and the virulent, disease-causing strains of the virus.

Dr Summa Bibby from UQ’s School of Chemistry and Molecular Bioscience said despite decades of research on yellow fever, this was the first time a complete 3D structure of a fully mature yellow fever virus particle had been recorded at near-atomic resolution.

“By utilising the well-established Binjari virus platform developed here at UQ, we combined yellow fever’s structural genes with the backbone of the harmless Binjari virus and produced virus particles that could be safely examined with a cryo-electron microscope,” Dr Bibby said.

Scientists Produce Powerhouse Pigment Behind Octopus Camouflage

An octopus camouflages itself with the seafloor. UC San Diego scientists have discovered a new way to produce large amounts of xanthommatin, a natural pigment used in animal camouflage, in a bacterium for the first time.
Photo Credit: Charlotte Seid

Scientists at UC San Diego have moved one step closer to unlocking a superpower held by some of nature’s greatest “masters of disguise.”

Octopuses, squids, cuttlefish and other animals in the cephalopod family are well known for their ability to camouflage, changing the color of their skin to blend in with the environment. This remarkable display of mimicry is made possible by complex biological processes involving xanthommatin, a natural pigment.

Because of its color-shifting capabilities, xanthommatin has long intrigued scientists and even the military, but has proven difficult to produce and research in the lab — until now.

New switch for programmed cell death identified

During the analysis work: Prof. Franz Hagn (left) and Dr. Umut Günsel
Photo Credit: Astrid Eckert / TUM 

In the fight against disease, programmed cell death – also known as apoptosis – is a key protective function of the body. It breaks down cells that are damaged or have undergone dangerous changes. However, cancer cells often manage to override this mechanism. A research team at the Technical University of Munich (TUM) has now succeeded in identifying a new molecular switch in this process and elucidating how it works.

The activation and deactivation of apoptosis is a promising field of research in basic biomedical research. The team led by Prof. Franz Hagn from the Chair of Structural Membrane Biochemistry at the TUM School of Natural Sciences has now discovered a new switch: "Many research teams worldwide are working on the exciting topic of apoptosis and its targeted control. The big advantage is that we are dealing with a highly efficient, evolutionarily developed regulatory mechanism. So, we don't have to invent something completely new, but can use the appropriate structural methods to learn from nature's optimized processes."

Researchers decipher a mechanism that determines the complexity of the glucocorticoid receptor

Above, from left to right, Pilar Montanyà-Vallugera, José Luis Torbado-Gardeazábal, Inés Montoya-Novoa and Montse Abella-Monleón. Below, from left to right, Alba Jiménez-Panizo, Pablo Fuentes-Prior, Eva Estébanez-Perpiñá and Andrea Alegre-Martí.
Photo Credit: Courtesy of University of Barcelona

Drugs to treat inflammatory and autoimmune diseases — such as asthma, psoriasis, rheumatoid arthritis or Chrousos syndrome — act mainly through the glucocorticoid receptor (GR). This essential protein regulates vital processes in various tissues, so understanding its structure and function at the molecular level is essential for designing more effective and safer drugs. Now, a study published in the journal Nucleic Acids Research (NAR) has revealed the mechanism of multimerization — the association of different molecules to form complex structures — of the glucocorticoid receptor, a process critical to its physiological function.

Deciphering how the GR forms oligomers — through the binding of several subunits — opens a crucial avenue for developing more selective drugs. These new drugs could modulate this association and thus minimize serious adverse effects, such as immunosuppression or bone loss.

Nanopore signals, machine learning unlocks new molecular analysis tool

Illustration of voltage-matrix nanopore profiling. The artistic rendering depicts proteins (colored shapes) being analyzed by solid-state nanopores under varying voltage conditions. By combining nanopore signals with machine learning, researchers can discriminate protein mixtures and detect changes in molecular populations.
Image Credit: ©2025 Sotaro Uemura, The University of Tokyo

Understanding molecular diversity is fundamental to biomedical research and diagnostics, but existing analytical tools struggle to distinguish subtle variations in the structure or composition among biomolecules, such as proteins. Researchers at the University of Tokyo have developed a new analytical approach, which helps overcome this problem. The new method, called voltage-matrix nanopore profiling, combines multivoltage solid-state nanopore recordings with machine learning for accurate classification of proteins in complex mixtures, based on the proteins’ intrinsic electrical signatures.

The study, published in Chemical Science, demonstrates how this new framework can identify and classify “molecular individuality” without the need for labels or modifications. The research holds promise of providing a foundation that could lead to more advanced and wider applications of molecular analysis in various areas, including disease diagnosis.

In a surprising discovery, scientists find tiny loops in the genomes of dividing cells

MIT experiments have revealed the existence of “microcompartments,” shown in yellow, within the 3D structure of the genome. These compartments are formed by tiny loops that may play a role in gene regulation.
Illustration Credit: Ed Banigan, edited by MIT News
(CC BY-NC-ND 4.0)

Before cells can divide, they first need to replicate all of their chromosomes, so that each of the daughter cells can receive a full set of genetic material. Until now, scientists had believed that as division occurs, the genome loses the distinctive 3D internal structure that it typically forms.

Once division is complete, it was thought, the genome gradually regains that complex, globular structure, which plays an essential role in controlling which genes are turned on in a given cell.

However, a new study from MIT shows that in fact, this picture is not fully accurate. Using a higher-resolution genome mapping technique, the research team discovered that small 3D loops connecting regulatory elements and genes persist in the genome during cell division, or mitosis.

“This study really helps to clarify how we should think about mitosis. In the past, mitosis was thought of as a blank slate, with no transcription and no structure related to gene activity. And we now know that that’s not quite the case,” says Anders Sejr Hansen, an associate professor of biological engineering at MIT. “What we see is that there’s always structure. It never goes away.”

The Many FACES of Lipid Research

Subcellular lipid distributions (magenta) in mitochondria (green) revealed using FACES and super-resolution structure illuminated microscopy.
Image Credit: William Moore

Lipids are fatty molecules that play critical roles in cell function, including membrane structure, energy storage and nutrient absorption. Most lipids are made in a cell organelle called the endoplasmic reticulum, but specific lipid types are shuttled around to different parts of the cell depending on their purpose. Each organelle serves a specific role in a cell and has its own unique mixture of lipids called a lipidome.

Scientists have long wanted to get a closer look at the movement of lipids around a cell, but because organelles are so close together – often only tens of nanometers apart – it’s tough to visualize with traditional light microscopy, which only has resolutions up to 250 nanometers.

Now researchers at the University of California San Diego have unveiled a new technology with the power to see cells in unprecedented detail. The tool, called fluorogen-activating coincidence encounter sensing (FACES), was developed in Associate Professor of Biochemistry & Molecular Biophysics Itay Budin’s lab. This work appears in Nature Chemical Biology.

Why women's brains face higher risk: scientists pinpoint X-chromosome gene behind MS and Alzheimer's

Image Credit: Scientific Frontline / AI generated

New research by UCLA Health has identified a sex-chromosome linked gene that drives inflammation in the female brain, offering insight into why women are disproportionately affected by conditions such as Alzheimer’s disease and multiple sclerosis as well as offering a potential target for intervention. 

The study published in the journal Science Translational Medicine, used a mouse model of multiple sclerosis to identify a gene on the X chromosome that drives inflammation in brain immune cells, known as microglia. Because females have two X chromosomes, as opposed to only one in males, they get a “double dose” of inflammation, which plays a major role in aging, Alzheimer’s disease and multiple sclerosis.  

When the gene, known as Kdm6a, and its associated protein were deactivated, the multiple sclerosis-like disease and neuropathology were both ameliorated with high significance in female mice.  

Cholesterol-lowering drugs could reduce the risk of dementia

Low cholesterol can reduce the risk of dementia, a new University of Bristol-led study with more than a million participants has shown.

The research, led by Dr Liv Tybjærg Nordestgaard while at the University of Bristol and the Department of Clinical Biochemistry at Copenhagen University Hospital – Herlev and Gentofte, found that people with certain genetic variants that naturally lower cholesterol have a lower risk of developing dementia.

The study, which is based on data from over a million people in Denmark, England, and Finland, has been published in the journal Alzheimer's & Dementia: The Journal of the Alzheimer's Association. 

Some people are born with genetic variants that naturally affect the same proteins targeted by cholesterol-lowering drugs, such as statins and ezetimibe. To test the effect of cholesterol-lowering medication on the risk of dementia, the researchers used a method called Mendelian Randomization — this genetic analysis technique allowed them to mimic the effects of these drugs to investigate how they influence the risk of dementia, while minimizing the influence of confounding factors like weight, diet, and other lifestyle habits.

Programmable proteins use logic to improve targeted drug delivery

Therapies that are sensitive to multiple biomarkers could allow medicines to reach only the areas of the body where they are needed. The diagram above shows three theoretical biomarkers that are present in specific, sometimes overlapping areas of the body. A therapy designed to find the unique area of overlap between the three will act on only that area.
Image Credit: DeForest et al./Nature Chemical Biology

Targeted drug delivery is a powerful and promising area of medicine. Therapies that pinpoint the exact areas of the body where they’re needed — and nowhere they’re not — can reduce the medicine dosage and avoid potentially harmful “off target” effects elsewhere in the body. A targeted immunotherapy, for example, might seek out cancerous tissues and activate immune cells to fight the disease only in those tissues.

The tricky part is making a therapy truly “smart,” where the medicine can move freely through the body and decide which areas to target.

DNA nanospring measures cellular motor power

Experimental design for the force measurement of KIF1A.
An inert protein known as KIF5B serves as the anchor from which KIF1A pulls the nanospring. As with more familiar springs, the extended length correlates with the force being applied. But in this case, the DNA nanospring is also labeled with fluorescent molecules which give away how far it stretches to make visualization of KIF1A’s motile strength possible.
Image Credit: ©2025 Hayashi et al
(CC BY-ND 4.0)

Cells all require the transport of materials to maintain their function. In nerve cells, a tiny motor made of protein called KIF1A is responsible for that. Mutations in this protein can lead to neurological disorders, including difficulties in walking, intellectual impairment and nerve degradation. It’s known that mutations in KIF1A also result in a weakened motor performance, but this has been difficult to measure so far. Researchers including those from the University of Tokyo and the National Institute of Information and Communications Technology (NICT) in Japan have measured changes in the force of KIF1A using a nanospring, a tiny, coiled structure, made of DNA which could lead to improved diagnosis of diseases related to the protein’s mutations.

Cell death in microalgae resembles that in humans

Under the microscope, it is possible to see for the first time how microalgae undergo the same type of programmed cell death as animal cells. (Microalgae in purple and apoptotic bodies as small dots.)
 Image Credit: Luisa Fernanda Corredor Arias

For the first time, researchers at Umeå University have observed the same type of programmed cell death in microalgae as in humans. The discovery, published in Nature Communications, shows that this central biological process is older than previously thought.

“This is the first photosynthetic organism, and the first single-cell organism, shown to produce so called apoptotic bodies during cell death. This proves that apoptosis, a pathway of programmed cell death which was thought to be unique to animals, is more ancient and widespread than previously believed,” says Christiane Funk, Professor at the Department of Chemistry, Umeå University.

Cells can die naturally from age or disease, but organisms can also actively trigger the death of certain cells when needed. This is known as programmed cell death (PCD), a central biological system that allows the development of organs in our bodies and provides advantage during an organism’s life cycle. One example is the differentiation of fingers in a developing human embryo; others are the control of cell numbers or the elimination of non-functional cells.

Early changes during brain development may hold the key to autism and schizophrenia

Photo Credit: Michal Jarmoluk

Researchers at the University of Exeter have created a detailed temporal map of chemical changes to DNA through development and aging of the human brain, offering new insights into how conditions such as autism and schizophrenia may arise.

The team studied epigenetic changes – chemical tags on our DNA that control how genes are switched on or off. These changes are crucial in regulating the expression of genes, guiding brain cells to develop and specialize correctly.

One important mechanism, called DNA methylation, was examined in nearly 1,000 donated human brains, spanning life from just six weeks after conception through to 108 years of age. The researchers focused on the cortex, a region of the brain involved in high-level functions such as thought, memory, perception, and behavior. Correct development of the cortex during early life is important to support healthy brain function after birth.

Possible breakthrough in the development of effective biomaterials

Professor Dr. Shikha Dhiman from the Department of Chemistry of JGU
Photo Credit: © Ankit Sakhuja

When model cell membranes bind to biomaterials, it is not the binding strength but the speed of the receptors in the membranes that is crucial

Many hopes rested on so-called tissue engineering: With the help of stem cells, skin and other organs could be grown, thereby enabling better wound healing and better transplants. Although some of this is already a reality, the level expected around 20 years ago has not yet been achieved because the stem cells do not always bind to the required host material as they should in theory. An international research team led by chemist Professor Shikha Dhiman from Johannes Gutenberg University Mainz (JGU) has now found the reason for this: "Whether an interaction between model cell membrane and matrix material occurs depends not only on the strength of the interaction but also on the speed at which the binding partner molecules move. The understanding of this interaction that we have now gained is crucial for the development of effective biomaterials," says Dhiman. The team's results were recently published in the renowned scientific journal PNAS.

Purdue biochemists discover self-repair function in key photosynthetic protein complex

Sujith Puthiyaveetil and Steve McKenzie look at a plant thylakoid in a lab at the biochemistry building at Purdue University.
Photo Credit: Purdue Agricultural Communications/Joshua Clark

Cyanobacteria began contributing oxygen to Earth’s mostly noxious atmosphere more than 2 billion years ago. The photosystem II protein complex now shared by various lineages of cyanobacteria, algae and land plants has served as a major site of oxygen production throughout the history of life on Earth ever since.

Ironically, receiving too much light can damage photosystem II and erode the photosynthetic efficiency of plants. Purdue University biochemists Steven McKenzie and Sujith Puthiyaveetil have gleaned new, long-hidden details about how photosystem II repairs itself. McKenzie and Puthiyaveetil’s findings have been published in the journal Plant Communications.

“The photosystem II splits water and extracts electrons and protons, leaving oxygen as a by-product. Photosystem II thereby powers life on Earth,” said Puthiyaveetil, associate professor of biochemistry. Even so, “it’s still fairly poorly understood how these huge protein complexes that use light energy to produce oxygen are able to be repaired and maintained so efficiently across different lineages of plants, algae and cyanobacteria.”

Research Pinpoints Weakness in Lung Cancer’s Defenses

A microscope image of lung cancer cells (purple) containing the activated form of a metabolic enzyme called GUK1 (brown) that supports cancer growth.
Image Credit: Haigis lab

Lung cancer is a particularly challenging form of cancer. It often strikes unexpectedly and aggressively with little warning, and it can shapeshift in unpredictable ways to evade treatment.

While researchers have gleaned important insights into the basic biology of lung cancer, some of the disease’s molecular maneuvers have remained elusive.

Now, a team led by scientists at Harvard Medical School has made strides in understanding how a genetic flaw in some lung cancers alters cancer cell metabolism to fuel the disease.

Working with mouse models and human cancer cells, the researchers identified a metabolic enzyme called GUK1 in lung cancers harboring an alteration in the ALK gene. Their experiments showed that GUK1 plays an important role in boosting metabolism in tumor cells to help them grow.

The findings, reported in Cell and supported in part by federal funding, provide a clearer picture of how metabolism works in lung cancer.

The research could set the stage for developing therapies that target GUK1 to curb cancer growth, the team said.

Discovery of unexpected collagen structure could ‘reshape biomedical research’

Jeffrey Hartgerink is a professor of chemistry and bioengineering at Rice.
Photo Credit: Courtesy of Jeffrey Hartgerink / Rice University

Collagen, the body’s most abundant protein, has long been viewed as a predictable structural component of tissues. However, a new study led by Rice University’s Jeffrey Hartgerink and Tracy Yu, in collaboration with Mark Kreutzberger and Edward Egelman at the University of Virginia (UVA), challenges that notion, revealing an unexpected confirmation in collagen structure that could reshape biomedical research.

The researchers used advanced cryo-electron microscopy (cryo-EM) to determine the atomic structure of a packed collagen assembly that deviates from the traditionally accepted right-handed superhelical twist. Published in ACS Central Science, the study suggests collagen’s structural diversity may be greater than previously believed.

“This work fundamentally changes how we think about collagen,” said Hartgerink, professor of chemistry and bioengineering. “For decades, we have assumed that collagen triple helices always follow a strict structural paradigm. Our findings show that collagen assemblies can adopt a wider range of conformations than previously thought.”

Spliceosome: How Cells Avoid Errors When Manufacturing Mrna

Quality control during splicing: When an error in the precursor mRNA is detected, the spliceosome is blocked, the recruited control factors interrupt the “normal” cycle, and a molecular short circuit causes the spliceosome to disassemble.
Image Credit: © K. Wild, K. Soni, I. Sinning

A complex molecular machine, the spliceosome, ensures that the genetic information from the genome, after being transcribed into mRNA precursors, is correctly assembled into mature mRNA. Splicing is a basic requirement for producing proteins that fulfill an organism’s vital functions. Faulty functioning of a spliceosome can lead to a variety of serious diseases. Researchers at the Heidelberg University Biochemistry Center (BZH) have succeeded for the first time in depicting a faultily “blocked” spliceosome at high resolution and reconstructing how it is recognized and eliminated in the cell. The research was conducted in collaboration with colleagues from the Australian National University.

New light-tuned chemical tools control processes in living cells

Jun Zhang, Laura Herzog and Yaowen Wu have found a way to control proteins in living cells.
Photo Credit: Shuang Li

A research group at Umeå University has developed new advanced light-controlled tools that enable precise control of proteins in real time in living cells. This groundbreaking research opens doors to new methods for studying complex processes in cells and could pave the way for significant advances in medicine and synthetic biology.

In our experiments, we were able to demonstrate precise control over several processes in the cell

“Cellular processes are complex and constantly change depending on when and where in the cell they occur. Our new chemical tool with light switches will make it easier to control processes in the cell and study how cells function in real time. We can also determine where we make such regulation with a resolution of micrometres within a cell or tissue”, says Yaowen Wu, professor at the Department of Chemistry and SciLifeLab Group leader at Umeå University.

The intricate choreography of what happens in a cell is based on the precise distribution and interaction of proteins over time and space. Controlling protein or gene function is a cornerstone of modern biological research. However, traditional genetic techniques such as CRISPR-Cas9 often operate on a longer time scale, which risks causing cells to adapt. In addition, the techniques lack the spatial and temporal precision required to study highly dynamic cellular processes.