Thursday, August 06, 2026

 

Butterfly lilies wing their way to Science




University of Cape Town - Faculty of Science
All the flowers on a individual Wachendorfia paniculata or Barberetta aurea, display either a left-morph or right morph phenotype. 

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A genetic switch determines left–right floral asymmetry in Wachendorfia and Barberetta mirror-image flowers

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Credit: Nicola Illing






The inner genetic secrets of how the flowers of butterfly lilies break left-right symmetry have been revealed for the first time in a paper published in the prestigious journal Science. An international team of scientists, including researchers and students from the University of Cape Town (UCT), has answered this century-old evolutionary curiosity, noted by an English naturalist and biologist Charles Darwin, nine days before his death, in a letter addressed to a professor of natural science at Tabor College, James E Todd, in America.

The study reveals, for the first time, the genetic and developmental mechanisms that determine the “handedness” of butterfly lilies (Wachendorfia), a genus of plants found only in South Africa’s Western and Eastern Cape and in a sister genus, Barberetta aurea found in KwaZulu-Natal and the Eastern Cape. The discovery sheds new light on one of biology’s most fundamental questions: How do living organisms break left-right symmetry during development?

Most animals and flowers are either radially or bilaterally symmetrical. Yet many organisms break this symmetry in remarkable ways. In humans, for example, the heart develops on the left side of the body. Butterfly lilies have evolved their own version of this phenomenon. Every flower on an individual plant develops with its female style pointing either to the left or to the right, while the central stamen deflects in the opposite direction. This ingenious arrangement reduces self-pollination and promotes efficient transfer of pollen between flowers of opposite orientation.

The research brought together scientists from UCT, the University of Potsdam and Wageningen University, with support from the Human Frontier Science Program and the South Africa 1KSA project. Researchers from UCT’s Department of Molecular and Cell Biology, together with postgraduate students, played a pivotal role in solving the puzzle.

“This study addresses a fascinating question that has puzzled evolutionary biologists for well over a century,” said Professor Nicola Illing from UCT’s Department of Molecular and Cell Biology. “By identifying the genes responsible for right-floral handedness, and conducting experiments on developing flower buds, we’ve uncovered the cues that determine how Wachendorfia and Barberetta flowers break symmetry, and whether a flower becomes left- or right-oriented.”

Research process

One of the project’s earliest hurdles was obtaining high-quality deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) from butterfly lilies, whose tissues are rich in sticky carbohydrates that complicate genetic studies. During her MSc research, Kelly Shepherd developed a protocol that successfully extracted high-quality genetic material from developing flower buds, laying the foundation for the team’s genomic analyses.

Comparing the DNA of hundreds of left- and right-oriented plants across four Wachendorfia species and B. aurea enabled the researchers to identify a segment of DNA found only in right-oriented plants. Further investigation revealed two closely linked genes, YUC-R and miR156, that switch the flower’s default left-oriented developmental programme into a right-oriented one before the style and stamen begin to bend.

UCT honours students Oliver Marketos and Anand Shankar provided further evidence by demonstrating that the butterfly lily version of miR156 performs the same regulatory function as the equivalent gene in the model plant Arabidopsis thaliana.

The team also embarked on a frenzied hunt across the Western Cape for naturally occurring butterfly lily mutants. Genetic analysis by Olivia Page-MacDonald demonstrated that these mutants were a natural test of the handedness genes’ function. When YUC-R was defective, the central stamen changed its deflection from left to the right, while if miR156 was defective, the style deflected to the left, instead of the right. These results provide compelling proof that YUC-R and miR156 control the flower’s handedness.

Significant discoveries

Professor Illing said one of the study’s most significant discoveries came unexpectedly. While recording flower development, she accidentally positioned a flower bud upside down. MSc student Caroline Robertson made the key observation that instead of continuing its normal growth, the developing flower reversed the orientation of its style and stamen.

“Scientific breakthroughs don’t always happen exactly as planned. This unexpected observation showed us that gravity provides an important directional cue as the flower develops. It was a remarkable moment that transformed our understanding of how these beautiful flowers establish their left-right orientation,” added Associate Professor Robert Ingle from UCT’s Department of Molecular and Cell Biology.

Beyond solving a long-standing evolutionary puzzle, the findings deepen scientists’ understanding of how genes, environmental signals and developmental processes interact to shape the extraordinary diversity of life.

As spring approaches, South Africans will have the opportunity to see these remarkable plants in bloom. The marsh butterfly lily (Wachendorfia thyrsiflora) grows along streams in the Western Cape and in botanical gardens around the world, while Wachendorfia brachyandra, Wachendorfia multiflora, and Wachendorfia paniculata can be found flowering across the Western Cape, from the Cederberg to Cape Agulhas, from August to November.


How asymmetric butterfly-lily flowers promote outcrossing [VIDEO] 

How asymmetric butterfly-lily flowers promote outcrossing


Animation illustrating how the transfer of pollen from a butterfly lily flower onto the wings of an insect ensures efficient pollen transfer between left- and right-morph flowers and vice versa. This is followed by live footage of a beefly (Australoechus hirtus) probing Wachendorfia paniculata flowers at Waylands, Darling, South Africa. Note how the wings beat against the opposing stamen and the style.

 

Credit

Nicola Illing and Olivia Page-MacDonald

 

 

Scientists discover a brain cycle that may explain why learning eventually stalls


UMD scientists found that a matrix surrounding brain cells loosens and rebuilds during learning—and gradually stops recurring once a skill is learned, offering new clues to why progress can grind to a halt




University of Maryland

perineuronal nets 

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Perineuronal nets—net-like structures that stabilize brain wiring (green)—surround parvalbumin-expressing neurons (magenta) in the gerbil auditory cortex.

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Credit: Dr. Jessica Winné.





For many who have struggled to learn a new language or instrument, it’s a familiar pattern: they make rapid progress at first, then hit a plateau that no amount of diligent practice or concentration seems to break.

University of Maryland biologists identified a physical mechanism in the brain that may help explain why such plateaus occur: a scaffold-like structure surrounding brain cells, called the extracellular matrix, helps control when the brain can change during learning. In the auditory cortex, this matrix loosens within hours of a practice session and rebuilds itself within about a day—a cycle that lets the learning from a session take hold before the next one. As a skill is mastered, the rebuilding cycle fades and eventually stops altogether, as if the brain has decided that learning is finished and it’s time to protect what’s been gained. The team published its findings in the Proceedings of the National Academy of Sciences on August 3, 2026.

“For the first time, we’ve been able to see that the remodeling process changes as you gain experience. It happens early in learning, declines and then gradually stops,” said the study’s senior author Melissa Caras, an assistant professor of biology at UMD. “This tells us that the brain isn’t just passively storing what you learn; it’s also actively regulating when learning can happen and when it should stop, so that the skills you’ve built are protected rather than overwritten.”

For decades, scientists viewed this matrix in adult brains as a rigid barrier, a scaffold that holds brain wiring in place and makes learning harder as we age. This helps to explain why young children pick up languages effortlessly while adults must work hard for every word. In early childhood, the dense, net-like structures that stabilize brain wiring are still immature, leaving the brain more open to change. As children grow older, the matrix matures and “firms up,” trading flexibility for stability.

While earlier studies caught glimpses of the matrix changing during learning as well, researchers only sampled occasionally (often over days or weeks) and concluded that it rebuilt slowly over long periods. Caras’s team tracked the cycle over much shorter intervals, resulting in findings that suggest that the adult matrix is far more dynamic. Rather than sitting fixed in place, the researchers found that the matrix shifts on a rapid rhythm tied to training—loosening after practicing a skill to acquire it and then knitting back together by the next day.

That speed matters because it means that the matrix loosens and resets on the same timescale as the training that drives learning. Each practice session gets its own opportunity for change, and the gains from one day settle in overnight to become the starting point for the next.

To test whether the extracellular matrix truly permits learning, the team used an enzyme to break down the matrix, which slowed learning. The more the matrix was disrupted, the greater the impairment—learning a skill and mastering it became more difficult. And when the matrix was broken down after a skill was successfully mastered, performance began to slip.

“Instead of being at your best, A-plus performance, you’re now working at a B-minus level,” Caras explained. “You don’t lose your skill completely, but mastery is noticeably eroding.”

While the team’s research is still in the early stages and far from direct human application, they believe the results open intriguing possibilities, especially for how we currently approach learning and retention. Based on the team’s findings, Caras theorized that plateaus in language learning could result from the brain regions involved flipping from a “ready to learn” state into a more stable one, with the matrix sealing the gains in place.

The team’s work may also have applications for hearing rehabilitation, and specifically, helping cochlear implant patients who have to train their brains to interpret an entirely new kind of signal, Caras explained.

“Someone newly fitted with a device might be more receptive to that training than a long-time user whose brain has already settled into a stable state,” Caras said. “If there’s a safe way to briefly reopen the learning window, it could be possible to help them acquire the skills to interpret these signals from their implant.”

The researchers are now working to identify the molecules that trigger changes to the matrix, record what the brain is doing during the brief window when the matrix loosens to learn, and explore the matrix’s role in hearing loss and related disorders.

“The catch is that the same matrix seems to be needed both to learn and to hold onto what’s learned,” she said. “The long-term hope is to learn how to temporarily open up this matrix at will to make the learning process more accessible.”

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The study, “Experience-dependent modulation of extracellular matrix integrity supports perceptual skill learning and memory,” was published in the Proceedings of the National Academy of Sciences on August 3, 2026.

This research was supported entirely by institutional start-up funds from the University of Maryland.

 

Low-fat vegan diet cuts dietary energy density by nearly a third, helping explain weight loss, new study finds





Physicians Committee for Responsible Medicine





WASHINGTON, D.C. — A low-fat vegan diet lowers the energy density of the foods people eat by roughly 30%, allowing them to eat satisfying amounts of food while taking in fewer calories and losing weight—without deliberately restricting calories—according to new research published in JAMA Network Open.

In a randomized clinical trial of adults with overweight, those who adopted an ad libitum low-fat vegan diet substantially reduced how many calories were packed into each gram of food they ate. That drop in energy density was linked to lower calorie intake and greater weight loss, even though participants were never told to eat less.

“This helps answer a question people often have about plant-based eating: How can you lose weight without counting calories or going hungry?” said Hana Kahleova, MD, PhD, director of clinical research at the Physicians Committee for Responsible Medicine and lead author. “The answer is energy density. Plant foods are rich in water and fiber, so you can fill your plate, feel full, and still take in fewer calories.”

A Mechanism Behind the Weight Loss

The analysis drew on a 16-week randomized trial in which adults with overweight were assigned to either an ad libitum low-fat vegan diet of fruits, vegetables, grains, and legumes, or a control group that made no dietary changes. Neither group was given calorie limits. Energy density was calculated for each participant as the ratio of total energy (kcal per day) to total food weight (grams per day).

Key findings include:

  • Total food weight did not change significantly in either group—participants on the vegan diet ate just as much food by weight.
  • Energy intake fell in both groups but more in the vegan group, by about 357 kcal/day.
  • Dietary energy density did not change in the control group but dropped about 30% in the vegan group.
  • Greater reductions in energy density were associated with greater weight loss, and the link held after accounting for changes in calorie intake.

Eat More Food, Take in Fewer Calories

The shift was driven by what landed on the plate. On the vegan diet, calorie-dense animal foods such as meat, dairy, and eggs were eliminated, while intake of high-volume, low-energy-density plant foods—especially vegetables and legumes—rose sharply. Because these foods carry few calories per gram, participants could eat generous portions while consuming less energy overall.

“This isn’t about willpower or smaller portions,” Dr. Kahleova said. “It’s about choosing foods that naturally deliver fewer calories in every bite. A 30% reduction in energy density is a substantial shift that would be very hard to achieve and sustain through portion control alone.”

Why Energy Density Matters

Energy density—the number of calories per gram of food—has long been studied as a driver of how much people eat. Controlled feeding studies show that lowering the energy density of meals helps people feel full and reduces how much they eat afterward, all while keeping the volume of food the same.

“When the foods you eat are lower in energy density, your body’s natural appetite signals work in your favor,” Dr. Kahleova said. “You eat until you’re satisfied, and you simply end up with fewer calories. That’s a sustainable way to manage weight.”

Implications for Weight Management

With dietary guidance often focused on cutting calories or controlling portions, the study points to a different and potentially more practical lever: the composition of the diet itself. Emphasizing water-rich, high-fiber plant foods may make it easier for people to reduce calorie intake without feeling deprived.

“From a clinical standpoint, targeting energy density offers a realistic strategy for weight loss,” Dr. Kahleova said. “Instead of telling people to eat less, we can help them eat differently—and the results follow.”

Bottom Line

A low-fat vegan diet substantially lowers dietary energy density, helping people take in fewer calories and lose weight without intentional calorie restriction.

“You don’t have to eat less,” Dr. Kahleova said. “You can eat more food, feel full, and still lose weight—by choosing foods that are naturally lower in energy density.”

Founded in 1985, the Physicians Committee for Responsible Medicine is a nonprofit organization that promotes preventive medicine, conducts clinical research, and encourages higher standards for ethics and effectiveness in education and research

 

Wearable fingertip sensor identifies physical patterns linked to stress and anxiety





Aston University





Researchers have shown that measurements taken from a person’s fingertip could help identify physical patterns associated with stress, anxiety and depression.

The international study, involving experts from Aston University, used a wearable device that shines light into the skin to measure blood flow through the smallest blood vessels as well as changes in the activity of the surrounding tissue.

These measurements were then combined with machine learning to investigate whether people reporting symptoms of stress, anxiety or depression displayed recognisable physical patterns.

The study involved 132 adults aged between 18 and 94 from across 19 countries. Participants completed a widely used 21-question assessment covering depression, anxiety and stress before undergoing repeated fingertip measurements.

The device examined how blood was flowing through the tiny vessels beneath the skin. It also measured substances associated with how cells produce and use energy, as well as skin temperature and heart rate.

Stress and anxiety can affect the nervous system, heart rate, circulation and metabolism, and scientists wanted to establish whether these effects could be detected through changes in the fingertip.

Machine-learning models were then used to compare the physical measurements with participants’ questionnaire results.

The models were able to distinguish, with moderate success, between people who reported stress-related symptoms and those who did not. Blood-flow patterns and measurements associated with tissue metabolism made an important contribution to the results.

Professor Edik Rafailov, from the Aston Institute of Photonic Technologies, jointly supervised the research and said the study provided early evidence that mental distress may be accompanied by measurable changes in the body.

He said:

“This study suggests that non-invasive photonic wearable technology can detect changes in blood flow and tissue activity through the skin that may provide useful information about a person’s stress-related symptoms.

“At present, mental health is generally assessed through conversations and questionnaires. These remain extremely important, but in the future physiological measurements could provide an additional source of information and help people monitor changes over time.

“This is an early proof-of-concept study, rather than a diagnostic test. We now need to test the approach with larger groups of participants and in clinical settings before we can determine how it might be used in practice.”

The technology does not currently diagnose depression, anxiety or any other mental health condition. Participants were classified using their answers to a questionnaire rather than diagnoses made by mental health professionals.

The researchers say the eventual aim would be to complement, rather than replace, existing mental health assessments.

The system could potentially help people and healthcare professionals monitor changes in wellbeing without requiring invasive medical tests. However, larger studies and independent clinical validation will be needed to establish its reliability across different populations and everyday environments.

The research also produced a dataset containing physiological measurements from a relatively diverse group of participants. This could help other researchers investigate the relationship between mental health, circulation and cellular activity.

The study, “A wearable device dataset for mental health assessment using laser Doppler flowmetry and fluorescence spectroscopy sensors”, has been published in the journal Communications Medicine.

The research involved Aston University, the Industrial University of Ho Chi Minh City, the University of Toronto, University Health Network in Toronto, Florida Institute of Technology, Pukyong National University, Stanford University, Hai Duong Central College of Pharmacy and the University of Alabama at Birmingham.

The work received support from the British Council Women in STEM Fellowships programme.

To read the full paper, visit https://doi.org/10.1038/s43856-026-01766-5 
 

  



 

Researchers create the most complete DNA profile of the brown rat to date





University of Texas Health Science Center at Houston

Peter Doris, PhD 

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Peter Doris, PhD, director of the Center for Human Genetics at The Brown Foundation Institute of Molecular Medicine within McGovern Medical School at UTHealth Houston.

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Credit: Photo by UTHealth Houston.






Researchers have created the most complete genetic profile of the brown rat to date, according to a UTHealth Houston-led team, paving the way for scientists to more accurately research the genetic links to conditions like heart disease, kidney disease, high blood pressure, and stroke. 

The research was published today in Cell Genomics and led by corresponding author Peter Doris, PhD, director of the Center for Human Genetics at The Brown Foundation Institute of Molecular Medicine within McGovern Medical School at UTHealth Houston.

The assembly of the brown rat’s genome provides a complete genetic fingerprint and reveals that the brown rat’s DNA is more complex than scientists previously understood. In addition to uncovering more than 60 new genes, many of which were previously difficult to sequence and are thought to play a role in immunity and other biological processes, the team discovered that brown rat sex chromosomes differ in a significant way from those in humans.

In humans, the X and Y chromosomes contain a region known as the pseudoautosomal region, or PAR, which plays a unique role in allowing the two dissimilar chromosomes to pair up and replicate. In most mammals, this region contains about 20 genes shared by both the X and Y chromosomes. This shared sequence is what allows these dissimilar chromosomes to match up and replicate. 

Doris and his team found that these PAR genes have been lost from the X and Y chromosomes in the brown rat, indicating rats use a different mechanism to reproduce. The team found that the PAR genes have moved to the regular chromosomes and uncovered new sequences that cause the X and Y chromosomes to pair head to tail, rather than head to head as in most other mammals.

“Sexual reproduction in the rat can take place, but it’s not taking place in exactly the same way that it is in humans,” said Doris, who is the Mary Elizabeth Holdsworth Distinguished University Chair in Metabolic and Inflammatory Disease Research. “We wouldn’t have been able to discern that if we hadn’t had this complete, high-quality, and accurate sequencing of the genome.”

The findings have important implications for healthcare research, as scientists will now have a more accurate starting point during preclinical studies that use the brown rat. 

“We know that there are genetic causes of diseases, but when we try to find out where in the genome they’re coming from, we kind of get lost,” Doris said. “Until now, it has been extremely difficult to recognize genetic differences because the assemblies that we were working with had missing pieces.”

Many of these pieces were regions in which genes have duplicated. The nearly identical copies could not be seen independently of each other prior to Doris’ work. Gene duplication is a key mechanism by which individual genomes, and the functions they encode, can differ.

The rat genome, or genetic fingerprint, is made up of 22 pairs of chromosomes, at each end of which is a sequence called a telomere. Doris’ research represents the first telomere-to-telomere assembly of the brown rat’s genome, providing complete, unbroken descriptions of each chromosome’s sequence.

Prior to this research, scientists were essentially trying to put together a complicated jigsaw puzzle without the photo you find on the puzzle box, Doris said. 

“If the puzzle doesn’t come with a picture on the box, and if there are a lot of pieces in there that just look like pieces of blue sky, it’s very hard to know where to put those pieces,” he said.

Using the long-read assembly method, Doris and his team were able to create eight different reference-quality genome assemblies, allowing scientists to better understand genetic variations among different brown rats and to track down the genetic variation contributing to disease. Like in humans, individual rat genomes are unique. That means that one rat’s genome, or jigsaw puzzle, will have pieces that another rat’s “puzzle” does not have.

The eight reference strains allowed the team to create what’s known as a pangenome, which allows scientists to compare the genomes of multiple rats simultaneously. This pangenome adds 7% more sequence to the genome of the rat species.

“You can go into any particular place around any particular gene that you’re interested in, say, the protease gene that’s involved in digesting your steak dinner. Is that gene going to be the same in all of these animals, or could it be different?” Doris said. “Turns out, in some rats, the gene is specialized to do one job in digestion and another one in the immune system. Each function resides in the original and a recently duplicated copy of the gene. The pangenome gives you one place to go where you can capture all of the major differences that you’re likely to encounter. That’s a very, very valuable tool to have.”

Yaming Zhu, a research assistant in the Center for Human Genetics at The Brown Foundation Institute of Molecular Medicine with McGovern Medical School, also served as an author on the study. 

Additional authors include: Theodore Samuel Kalbfleisch, PhD; Julia L. Ciosek, MS; and Kai Li of the University of Kentucky; Sergey Koren, PhD; Adam Phillippy, PhD; Brandon Pickett, PhD; Gerard Bouffard, PhD; and Shelise Y. Brooks of the National Institutes of Health; Melissa Smith, PhD; and William A. Lauer of the University of Louisville; and Beth Dumont, PhD, of The Jackson Laboratory.