Gut-brain communication turned on its axis

How the gut communicates with the brain
Image Credit: Copilot AI

The mechanisms by which antidepressants and other emotion-focused medications work could be reconsidered due to an important new breakthrough in the understanding of how the gut communicates with the brain.

New research led by Flinders University has uncovered major developments in understanding how the gut communicates with the brain, which could have a profound impact on the make-up and use of medications such as antidepressants.

“The gut-brain axis consists of complex bidirectional neural communication pathway between the brain and the gut, which links emotional and cognitive centers of the brain,” says Professor Nick Spencer from the College of Medicine and Public Health.

“As part of the gut-brain axis, vagal sensory nerves relay a variety of signals from the gut to the brain that play an important role in mental health and wellbeing.

“The mechanisms by which vagal sensory nerve endings in the gut wall are activated has been a major mystery but remains of great interest to medical science and potential treatments for mental health and wellbeing.”

Human stem cells coaxed to mimic the very early central nervous system

Jianping Fu, Ph.D., Professor of Mechanical Engineering at the University of Michigan and the corresponding author of the paper being published at Nature discusses his team’s work in their lab with Jeyoon Bok, Ph.D. candidate at the Department of Mechanical Engineering.
Photo Credit: Marcin Szczepanski, Michigan Engineering

The first stem cell culture method that produces a full model of the early stages of the human central nervous system has been developed by a team of engineers and biologists at the University of Michigan, the Weizmann Institute of Science, and the University of Pennsylvania.

“Models like this will open doors for fundamental research to understand early development of the human central nervous system and how it could go wrong in different disorders,” said Jianping Fu, U-M professor of mechanical engineering and corresponding author of the study in Nature.

The system is an example of a 3D human organoid—stem cell cultures that reflect key structural and functional properties of human organ systems but are partial or otherwise imperfect copies.

“We try to understand not only the basic biology of human brain development, but also diseases—why we have brain-related diseases, their pathology, and how we can come up with effective strategies to treat them,” said Guo-Li Ming, who along with Hongjun Song, both Perelman Professors of Neuroscience at UPenn and co-authors of the study, developed protocols for growing and guiding the cells and characterized the structural and cellular characteristics of the model.

Vaping can increase susceptibility to infection by SARS-CoV-2

UC Riverside study urges e-cigarette users to be cautious about vaping in the era of COVID-19
Photo Credit: Karl Edwards

Vapers are susceptible to infection by SARS-CoV-2, the virus that spreads COVID-19 and continues to infect people around the world, a University of California, Riverside, study has found.

The liquid used in electronic cigarettes, called e-liquid, typically contains nicotine, propylene glycol, vegetable glycerin, and flavor chemicals. The researchers found propylene glycol/vegetable glycerin alone or along with nicotine enhanced COVID-19 infection through different mechanisms.  

The researchers also found that the addition of benzoic acid to e-liquids prevents the infection caused by propylene glycol, vegetable glycerin, and nicotine. 

“Users who vape aerosols produced from propylene glycol/vegetable glycerin alone or e-liquids with a neutral to basic pH are more likely to be infected by the virus, while users who vape aerosols made from e-liquids with benzoic acid — an acidic pH — will have the same viral susceptibility as individuals who do not vape,” said Rattapol Phandthong, a postdoctoral researcher in the Department of Molecular, Cell and Systems Biology and the research paper’s first author.

The researchers obtained airway stem cells from human donors to produce a 3D tissue model of human bronchial epithelium. They then exposed the tissues to JUUL and BLU electronic cigarette aerosols to study the effect on SARS-CoV-2 infection. They found all tissues showed an increase in the amount of ACE2, a host cell receptor for the SARS-CoV-2 virus. Further, TMPRSS2, an enzyme essential for the virus to infect cells, was found to show increased activity in tissues exposed to aerosols with nicotine.

Study sheds light on how neurotransmitter receptors transport calcium, a process linked with origins of neurological disease

Illustration Credit: Courtesy of McGill University

A new study from a team of McGill University and Vanderbilt University researchers is shedding light on our understanding of the molecular origins of some forms of autism and intellectual disability.

For the first time, researchers were able to successfully capture atomic resolution images of the fast-moving ionotropic glutamate receptor (iGluR) as it transports calcium. iGluRs and their ability to transport calcium are vitally important for many brain functions such as vision or other information coming from sensory organs. Calcium also brings about changes in the signaling capacity of iGluRs and nerve connections which are a key cellular events that lead to our ability to learn new skills and form memories.

iGluRs are also key players in brain development and their dysfunction through genetic mutations has been shown to give rise to some forms of autism and intellectual disability. However, basic questions about how iGluRs trigger biochemical changes in the brain’s physiology by transporting calcium have remained poorly understood.

In the study, the researchers took millions of snapshots of the iGluR protein in the act of transporting calcium, and unexpectedly discovered a temporary pocket that traps calcium on the outside of the protein. With this information at hand, they then used high-resolution electrophysiological recordings to watch the protein in motion as it transported calcium into the nerve cell.

Scientists assemble a richer picture of the plight and resilience of the foothill yellow-legged frog

Foothill yellow-legged frogs live in the flowing water of rivers and streams, so are especially vulnerable when these shrink to isolated pools.
Photo Credit: Brome McCreary / USGS

Up to only a few inches in length, with a lemon-hued belly, the foothill yellow-legged frog may seem unassuming. But its range once stretched from central Oregon to Baja California. In 2023, it was listed under the federal Endangered Species Act. Its rapidly decreasing range is due in part to a fungal pathogen called Batrachochytrium dendrobatidis, or Bd, that has devastated amphibians around the world.

A team of researchers, including UC Santa Barbara’s Andrea Adams, has conducted the most comprehensive study to date of disease dynamics in foothill yellow-legged frogs. The team’s data — sourced from both wild frogs and specimens in museum collections — enabled them to track patterns of infection across a large geographic range. In a study published in Royal Society Open Science, the researchers reveal that drought, rising temperatures and the increasing conversion of land for agriculture appear to be the largest factors driving Bd infection in this species.

The researchers aimed to assemble as much data as they could, both in space and time. They surveyed in the creeks and rivers of California and Oregon, where they swabbed wild yellow-legged frogs for the presence of Bd. It also led them into fluorescent-lit museum collections to sample specimens from as far back as the 1890s.

Vanishing Forests and Suffering Children: The Hidden Toll of Deforestation in Cambodia

Deforestation is suspected to have adverse impacts on child health. Investigating this phenomenon in Cambodia, a recent study sheds light on the devastating impact of prenatal exposure to deforestation on child health in Cambodia. The study reveals that children born in areas with recent deforestation suffer from lower birth weights and stunted growth. Moreover, pregnant women exposed to deforestation are more likely to experience anemia. These findings underscore the urgent need for effective targeted policies.

Deforestation, a critical consequence of human activity, has garnered significant attention due to its impact on environmental sustainability, biodiversity and climate change. However, an equally pressing yet less explored aspect is the relationship between deforestation and human health, especially in impoverished regions. Scientists have increasingly recognized the detrimental effects of deforestation on various aspects of human health, particularly among children. Studies reveal that children residing in areas with high deforestation rates are at an elevated risk of malaria, respiratory illnesses, diarrheal diseases, and malnutrition. This is particularly alarming given that these regions are often home to the most economically disadvantaged populations, worsening existing health disparities.

An increase in blood-sucking black flies is expected in Germany

Simulium ornatum is a black fly species of veterinary and human medical relevance.
Photo Credit: Dorian Dörge

Researchers from Goethe University Frankfurt and the Senckenberg Biodiversity and Climate Research Centre have modeled the spatial distributional patterns of black flies in Hesse, North Rhine-Westphalia, Rhineland-Palatinate and Saxony for the first time. In the study published in the renowned journal Science of the Total Environment, the research team shows that black flies in Germany can be categorized into three groups with different distribution patterns and ecological requirements. The researchers point out that medically relevant species in particular could become more prevalent as a result of ongoing climate and land-use change. 

Only six millimeters in length, black flies (Simuliidae) may look harmless like house flies, but their bites can be very unpleasant. Similar to mosquitoes, the females of these insects that are able to fly need a blood meal to produce eggs. Known as “pool feeders", they use their sharp “teeth" to scratch the skin of the host and then ingest the resulting drop of blood. “The anticoagulant and anesthetic substances introduced into the wound by mosquitoes can trigger serious allergic reactions or lead to secondary bacterial infections," states Prof. Dr. Sven Klimpel from the Senckenberg Biodiversity and Climate Research Centre, Goethe University Frankfurt, the LOEWE Centre for Translational Biodiversity Genomics (TBG), and the Fraunhofer IME Giessen. Klimpel continues: "Black flies are also vector-competent, meaning they are able to transmit pathogens that cause infectious diseases through their bites." One of the most well-known diseases transmitted by black flies is onchocerciasis, also known as “river blindness", caused by the nematode Onchocerca volvulus, which is native to Africa. According to the World Health Organization, more than 1.15 million people worldwide have already lost their sight as a result of the disease. 

Study shows orchid family emerged in northern hemisphere and thrived alongside dinosaurs

Phallaenopsis orchid in bloom
Photo Credit: John Wiesenfeld

Scientists at the Royal Botanic Gardens in Kew and the University of Portsmouth, along with partners in Latin America, Asia and Australia, have presented an updated family tree of orchids, tracing their origins to the northern hemisphere some 85 million years ago.

The study, published in leading journal New Phytologist, sheds new light on their complex and fascinating evolutionary history, and the authors hope their findings will help inform future orchid conservation planning. 

The orchid family, Orchidaceae, is often lauded by scientists as one of the greatest evolutionary marvels within the plant world. Not only are these flowering plants found on every continent except the Antarctic and in virtually every habitat, including north of the Arctic Circle, but they are also incredibly diverse, with an estimated 29,500 species – nearly three times more than the recognized number of bird species globally.  

It is generally accepted that orchids originated as far back as around 90 million years or more ago, but they were previously thought to have emerged on the supercontinent Gondwana, in what is present-day Australia.

However, the new study indicates their common ancestor may have originated in the northern hemisphere, on the supercontinent Laurasia, before spreading out further into the world.  

3D model: This is how the body’s building blocks are made

Using electron microscopy, scientists have managed to produce a 3D model of a part of the human cell, the ribosome, which is no more than 30 nanometers in diameter.
Graphic Credit: Eva Kummer

Human cells contain ribosomes, a complex machine that produces proteins for the rest of the body. Now the researchers have come closer to understanding how the ribosome works.

“It is amazing that we can visualize the atomic details of the ribosome. Because they are tiny – around 20-30 nanometers.”

So says Associate Professor Eva Kummer from the Novo Nordisk Foundation Center for Protein Research, who is responsible for the new study published in Nature Communications.

And don’t worry if you don’t know how much a nanometer is. It is around one billionth of a meter.

Using electron microscopy, Eva Kummer and her colleagues Giang Nguyen and Christina Ritter have managed to produce a 3D model of a part of the human cell, the ribosome, which is no more than 30 nanometers in diameter.

More specifically, they have taken snapshots of how a ribosome is made.

“It is important to understand how the ribosome is built and how it works, because it is the only cell particle that produces proteins in humans and all other living organisms. And without proteins, life would cease to exist,” says Eva Kummer.

Proteins are the primary building blocks of the human body. Your heart, lungs, brain and basically your whole body is made of proteins produced by the ribosome.

“From the outside, the human body looks pretty simple, but then consider the fact that every part of the body consists of millions of molecules, that are extremely complex, and that they all know what to do – that is pretty breathtaking,” says Eva Kummer.

Mice study suggests metabolic diseases may be driven by gut microbiome, loss of ovarian hormones

Mice that received fecal implants from donors that had their ovaries removed gained more fat mass and had greater expression of liver genes associated with inflammation, Type 2 diabetes, fatty liver disease and atherosclerosis. The findings may shed light on the greater incidence of metabolic dysfunction in postmenopausal women. The team members included, from left: molecular and integrative physiology professor Erik R. Nelson; Kelly Swanson, the director of the Division of Nutritional Sciences and the Kraft Heinz Endowed Professor in Human Nutrition; and animal sciences professor Brett R. Loman.
  Photo Credit: Fred Zwicky

The gut microbiome interacts with the loss of female sex hormones to exacerbate metabolic disease, including weight gain, fat in the liver and the expression of genes linked with inflammation, researchers found in a new rodent study.

The findings, published in the journal Gut Microbes, may shed light on why women are at significantly greater risk of metabolic diseases such as obesity and Type 2 diabetes after menopause, when ovarian production of female sex hormones diminishes.

“Collectively, the findings demonstrate that removal of the ovaries and female hormones led to increased permeability and inflammation of the gut and metabolic organs, and the high-fat diet exacerbated these conditions,” said Kelly S. Swanson, the director of the Division of Nutritional Sciences and the Kraft Heinz Endowed Professor in Human Nutrition at the University of Illinois Urbana-Champaign who is a corresponding author of the paper.  “The results indicated that the gut microbiome responds to changes in female hormones and worsens metabolic dysfunction.”

Stopping the awakening of leukemia stem cells to prevent relapse

Acute Myeloid Leukemia
Image Credit: National Cancer Institute

Why myeloid leukemias start to grow again after chemotherapy has killed the bulk of cancerous cells, and how growth may be blocked by repurposed drugs, may have been solved by new research.

The bone marrow of Acute Myeloid Leukemia (AML) patients contains a rare population of leukemic stem cells (LSCs) that do not grow and, therefore, are not killed by chemotherapy.

However, after treatment, these cells start to grow and produce AML cells, but it has until now been unclear as to what kick-starts this process.

In a new study, published in Nature Communications, experts from Newcastle University, the University of Birmingham and the Princess Maxima Centre of Pediatric oncology, studied single cells from patients with t(8;21) AML to investigate what made the rare LSCs grow.

Caring glass frog fathers have smaller testes

Males of the glassfrog species Hyalinobatrachium valerioi are very dedicated fathers.
Photo Credit: © Francesca Angiolani

An international team of researchers including the University of Bern shows in a new study that male glass frogs that care for their offspring have smaller testes than males of species that do not provide any brood care. This indicates an evolutionary trade-off between sperm production and parenting.

Living in the tropical rainforests of Central and South America, frogs of the glass frog family are fascinating because of their transparent skin on their belly, which reveals their internal organs. However, it is not only the appearance of these amphibians that is remarkable, but also their social behavior. In many - but not all - glass frog species, the males remain with the clutch after mating and guard and care for their offspring. In a new study, an international team, including researchers from the Institute of Ecology and Evolution at the University of Bern, shows that there is a link between this paternal care and the testes size of glass frogs. The results were recently published in the journal Proceedings of the Royal Society B.

How Does the Brain Make Decisions?

Image Credit: Generated by HM News with AI in Adobe Firefly

Scientists have gained new insights into how neurons in the brain communicate during a decision, and how the connections between neurons may help reinforce a choice.

The study — conducted in mice and led by neuroscientists at Harvard Medical School — is the first to combine structural, functional, and behavioral analyses to explore how neuron-to-neuron connections support decision-making.

“How the brain is organized to help make decisions is a big, fundamental question, and the neural circuitry — how neurons are connected to one another — in brain areas that are important for decision-making isn’t well understood,” said Wei-Chung Allen Lee, associate professor of neurobiology in the Blavatnik Institute at HMS and professor of neurology at Boston Children’s Hospital. Lee is co-senior author on the paper with Christopher Harvey, professor of neurobiology at HMS, and Stefano Panzeri, professor at University Medical Center Hamburg-Eppendorf.

In the research, mice were tasked with choosing which way to go in a maze to find a reward. The researchers found that a mouse’s decision to go left or right activated sequential groups of neurons, culminating in the suppression of neurons linked to the opposite choice.

These specific connections between groups of neurons may help sculpt decisions by shutting down neural pathways for alternative options, Lee said.

Possible trigger for autoimmune diseases discovered

 One of the great mysteries of immunology: the function of B cells (green) in the thymus gland was previously unknown. Researchers have now been able to show that the immune cells help to prevent T cells from attacking the body.
Image Credit: Jan Böttcher, Thomas Korn / TUM

Immune cells must learn not to attack the body itself. A team of researchers from the Technical University of Munich (TUM) and the Ludwig Maximilian University of Munich (LMU) has discovered a previously unknown mechanism behind this: other immune cells, the B cells, contribute to the "training" of the T cells in the thymus gland. If this process fails, autoimmune diseases can develop.

In children and adolescents, the thymus gland functions as a "school for T cells". The organ in our chest is where the precursors of those T cells that would later attack the body's own cells are discarded. Epithelial cells in the thymus present a large number of molecules that occur in the body to the future T cells. If any of them reacts to one of these molecules, a self-destruction program is triggered. T cells that attack the body's own molecules remaining intact and multiplying, on the other hand, can cause autoimmune diseases.

New mechanism discovered

In Nature, the team led by Thomas Korn, Professor of Experimental Neuroimmunology at TUM and a Principal Investigator in the SyNergy Cluster of Excellence, and Ludger Klein, Professor of Immunology at LMU’s Biomedical Center (BMC), describe another previously unknown mechanism behind this.

In addition to the precursors of T cells, the thymus gland also contains other immune cells, the B cells. They develop in the bone marrow but migrate to the thymus in early childhood. "The function of B cells in the thymus gland has been a mystery that has puzzled immunologists for many years," says Thomas Korn. The researchers have now been able to show for the first time that B cells play an active role in teaching T cells which targets not to attack.

False Alarm of the Immune System during Muscle Disease

Prof. Claudia Günther (left) from Dresden and Prof. Eva Bartok (right) from Bonn are jointly investigating the connection between myotonic dystrophy and autoimmune diseases.
Photo Credit: © Universitätsklinikum Dresden & Universitätsklinikum Bonn

Researchers at the University Hospitals of Dresden and Bonn of the DFG Transregio 237 and from the Cluster of Excellence ImmunoSensation2 at the University of Bonn have made progress clarifying why patients with myotonic dystrophy 2 have a higher tendency to develop autoimmune diseases. Their goal is to understand the development of the disease, and their research has provided new, potential therapeutic targets. The results of the study have now been published in the renowned journal Nature Communications.

Myotonic dystrophy 2 (DM2) is a form of muscular dystrophy, a disease that leads to progressive muscle degeneration. It is caused by the expansion of a repetitive DNA sequence containing multiple CCTG bases in the CNBP gene. In general, the sequence of nucleobases in the DNA carries the genetic information. Patients suffer from muscle weakness that is more pronounced in the area of the muscles close to the trunk, as well as sustained muscle stiffness and pain. Although DM2 occurs in roughly one out of 10,000 people in Germany, there are no targeted therapies. In initial studies, Prof. Claudia Günther and her team at the Carl Gustav Carus University Hospital at the Technical University of Dresden also observed that patients with DM2 suffer more from autoimmune diseases with an increased production of antibodies in the blood than the general population. However, the underlying mechanism for these symptoms was previously unknown.

Mitochondrial activation in transplanted cells promotes regenerative therapy for heart healing

Regenerative therapy to treat heart failure is more effective when the mitochondria of the regenerative cells are activated prior to treatment.
Image Credit: Gemini Advance

Heart failure stands as a leading cause of mortality worldwide, demanding advanced treatment options. Despite the urgency for more effective treatments, options for severe heart failure remain limited. Cell transplantation therapy has emerged as a promising ray of hope, as it can be used in regenerative therapy to heal the heart.

A research team led by Professor Yuma Yamada of Hokkaido University’s Faculty of Pharmaceutical Science has developed a technique to promote cardiac regeneration by delivering mitochondrial activators to cardiac progenitor cells. Their findings were published in the Journal of Controlled Release.

“Cardiomyocytes efficiently use the mitochondrial tricarboxylic acid cycle to produce large amounts of adenosine triphosphate from several substrates via oxidative phosphorylation (OXPHOS),” explains Yamada. “Based on the energy metabolism of cardiomyocytes, we hypothesized that activating the mitochondrial function of transplanted cells may improve the outcome of cell transplantation therapy.”

Learning How Cells Dispose of Unwanted Materials is Key to Potential New Therapeutics

Gary Kleiger, UNLV professor and chair of the department of chemistry and biochemistry in the College of Sciences.
Photo Credit: Lonnie Timmons III / University of Nevada, Las Vegas

Are you sick and tired of getting sick and tired? A UNLV-led research team is exploring whether the reason we sometimes feel ill in the first place is because our body’s cells suffer from trash that accumulates within them.

Gary Kleiger, professor and chair of the department of chemistry and biochemistry at UNLV, along with Brenda Schulman, director of the Munich-based Max Planck Institute of Biochemistry, and their teams are working on ways to help our bodies hunt down and destroy disease-causing proteins. They’re the authors of a groundbreaking new study published Feb. 20 in the journal Molecular Cell that furthers our understanding of how enzymes called cullin-RING ligases (or CRLs) help cells get rid of proteins that are no longer needed. The results also point to a potential Achilles heel for proteins that make us ill. 

“Cullin-RING-ligases (CRLs) are complex nanomachines that are crucial for the cell’s intricate disposal and recycling systems,” said Schulman. “CRLs tag defective, toxic, or superfluous proteins with a small protein called ubiquitin, and mutations or malfunctions impairing CRLs are often associated with diseases, like developmental disorders or cancers.” 

Magnetic effects at the origin of life?

Biomolecules such as our genetic material, DNA, basically exist in two mirror-image forms; however, all living organisms only ever use one of them. Why this is the case is still unclear.
Image Credit: Gemini Advance

It's the spin that makes the difference

Biomolecules such as amino acids and sugars occur in two mirror-image forms – in all living organisms, however, only one is ever found. Why this is the case is still unclear. Researchers at Empa and Forschungszentrum Jülich in Germany have now found evidence that the interplay between electric and magnetic fields could be at the origin of this phenomenon.

The so-called homochirality of life – the fact that all biomolecules in living organisms only ever occur in one of two mirror-image forms – has puzzled a number of scientific luminaries, from the discoverer of molecular chirality, Louis Pasteur, to William Thomson (Lord Kelvin) and Nobel Prize winner Pierre Curie. A conclusive explanation is still lacking, as both forms have, for instance, the same chemical stability and do not differ from each other in their physico-chemical properties. The hypothesis, however, that the interplay between electric and magnetic fields could explain the preference for one or the other mirror-image form of a molecule – so-called enantiomers – emerged early on.

It was only a few years ago, though, that the first indirect evidence emerged that the various combinations of these force fields can indeed "distinguish" between the two mirror images of a molecule. This was achieved by studying the interaction of chiral molecules with metallic surfaces that exhibit a strong electric field over short distances. The surfaces of magnetic metals such as iron, cobalt or nickel thus allow electric and magnetic fields to be combined in various ways – the direction of magnetization is simply reversed, from "North up – South down" to "South up – North down". If the interplay between magnetism and electric fields actually triggers "enantioselective" effects, then the strength of the interaction between chiral molecules and magnetic surfaces should also differ, for example – depending on whether a right-handed or left-handed molecule "settles" on the surface.

Where Neural Stem Cells Feel at Home

In the laboratory, the Bochum researchers are investigating which environment offers neural stem cells the best chances of survival.
Photo Credit: © RUB, Marquard

Injuries in the central nervous system heal poorly because cavities scar. Researchers hope to remedy this problem by filling the cavities in such a way that stem cells feel comfortable in them.

Researchers from Bochum and Dortmund have created an artificial cell environment that could promote the regeneration of nerves. Usually, injuries to the brain or spinal cord don’t heal easily due to the formation of fluid-filled cavities and scars that prevent tissue regeneration. One starting point for medical research is therefore to fill the cavities with a substance that offers neural stem cells optimal conditions for proliferation and differentiation. The team from Ruhr University Bochum and TU Dortmund University, both in Germany, showed that positively charged hydrogels can promote the survival and growth of stem cells.

Dr. Kristin Glotzbach and Professor Andreas Faissner from the Department of Cell Morphology and Molecular Neurobiology in Bochum cooperated with Professor Ralf Weberskirch and Dr. Nils Stamm from the Faculty of Chemistry and Chemical Biology at TU Dortmund University. The team describes the findings in the American Chemical Society Journal Biomaterials Science and Engineering.

Discovery about bacterial cell walls can lead to new antibiotics

Felipe Cava is Professor of Infection Biology, Department of Molecular Biology, Umeå University and affiliated group leader with the Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå Centre for Microbial Research (UCMR) and the Integrated Science Lab (Icelab) and SciLifeLab.
Photo Credit: Mattias Pettersson, simon ohman jonsson inhousebyran

Researchers at Umeå University in Sweden, led by Professor Felipe Cava, have identified a new family of enzymes that creates a unique type of cross-linking between the building blocks of bacterial cell walls. This discovery could help develop new antibiotics against infectious diseases.

Bacterial cell walls form mesh-like structures, shielding cells from rupturing under high internal pressure and safeguarding against external threats. The cell wall is comprised of sugar and amino acid molecules interconnected by various types of cross-links. These cross-links play a crucial role in providing strength and stability to the cell wall, while also enabling bacteria to adapt to diverse environments and stressors.

In a groundbreaking study recently published in the esteemed journal Nature Communications, researchers from Umeå University and international institutions have unveiled a novel family of enzymes responsible for generating a unique cross-linkage between L-alanine and meso-diaminopimelic acid. These amino acids are integral components of the peptide chains constituting the cell wall of numerous bacterial species. Termed LD1,3-transpeptidase, this enzyme has been identified across various groups of alpha and beta proteobacteria, including opportunistic pathogens such as Burkholderia and Achromobacter.