Scratching an itch promotes antibacterial inflammation

Summary author: Walter Beckwith

American Association for the Advancement of Science (AAAS)

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New research uncovers the dual nature of scratching an itch; although it can worsen skin inflammation, it can also boost immune defenses against bacterial infections at the injury site. The findings shed light on a pharmacologically targetable pathway that explains how scratching triggers inflammation, resolving the paradox of scratching as both a harmful pathological process and a beneficial evolutionary adaptation. Scratching is a natural, instinctive response to the sensation of itching, and it plays a central role in many skin conditions and injuries, such as dermatitis and insect bites, where chronic itching can be a major source of discomfort. Scratching can aggravate the condition by promoting inflammation in a self-perpetuating "itch-scratch cycle," where the scratching intensifies the itch and can exacerbate the injury. Yet unlike pain, which typically causes an aversion response, scratching can feel pleasurable, which suggests it might serve some adaptive benefit. However, the mechanisms by which scratching contributes to skin inflammation and whether the itch-scratch reflex offers any benefits to the host remain poorly understood. Using a novel genetically modified mouse model, Andrew Liu and colleagues explored how eliminating the function of itch-sensing neurons called nonpeptidergic 2 (NP2) affects the connection between itch, scratch and inflammation. Liu et al. discovered that scratching activates pain-sensing neurons that release substance P (SP), which stimulates mast cells to increase inflammation, mainly by attracting neutrophils. However, while scratching can aggravate issues like dermatitis, it may also help host immune defense by reducing bacteria, such as Staphylococcus aureus, during infections. Moreover, scratching can influence the skin's microbiome at the injury site, potentially preventing microbiota imbalances, although chronic conditions like atopic dermatitis complicate this. According to the authors, the findings suggest that scratching serves both as a pathological driver of inflammation and an evolutionary mechanism to bolster protection against infection. “Beyond defining a previously unidentified neuroimmune itch-scratch circuit, the findings of Liu et al. may lay a foundation for discoveries to help people suffering from chronic itch,” writes Aaron Ver Heul in a related Perspective.

 

Podcast: A segment of Science's weekly podcast with Daniel Kaplan, related to this research, will be available on the Science.org podcast landing page after the embargo lifts. Reporters are free to make use of the segments for broadcast purposes and/or quote from them – with appropriate attribution (i.e., cite "Science podcast"). Please note that the file itself should not be posted to any other Web site.

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Journal

Science

DOI

10.1126/science.adn9390 

Article Title

Scratching promotes allergic inflammation and host defense via neurogenic mast cell activation

Article Publication Date

31-Jan-2025

 

Why you shouldn’t scratch an itchy rash: New study explains

University of Pittsburgh

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Daniel Kaplan, M.D., Ph.D., professor of dermatology and immunology at the University of Pittsburgh

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Credit: Nate Langer, UPMC

Your parents were right: Scratching an itchy rash really does make it worse. Now we know why, thanks to new research published today in the journal Science that uncovers how scratching aggravates inflammation and swelling in a mouse model of a type of eczema called allergic contact dermatitis.

“At first, these findings seemed to introduce a paradox: If scratching an itch is bad for us, why does it feel so good?” said senior author Daniel Kaplan, M.D., Ph.D., professor of dermatology and immunology at the University of Pittsburgh. “Scratching is often pleasurable, which suggests that, in order to have evolved, this behavior must provide some kind of benefit. Our study helps resolve this paradox by providing evidence that scratching also provides defense against bacterial skin infections.”

Allergic contact dermatitis is an allergic reaction to allergens or skin irritants — including poison ivy and certain metals such as nickel — leading to an itchy, swollen rash. Succumbing to the often-irresistible urge to scratch triggers further inflammation that worsens symptoms and slows healing.

To figure out what drives this vicious cycle, Kaplan, first author Andrew Liu, student in Pitt’s Medical Scientist Training Program, and their team used itch-inducing allergens to induce eczema-like symptoms on the ears of normal mice and those that don’t get itchy because they lack an itch-sensing neuron.

When normal mice were allowed to scratch, their ears became swollen and filled with inflammatory immune cells called neutrophils. In contrast, inflammation and swelling were much milder in normal mice that couldn’t scratch because they wore tiny Elizabethan collars, similar to a “cone of shame” that a dog might sport after a visit to the vet, and in animals that lacked the itch-sensing neuron. This experiment confirmed that scratching further aggravates the skin.

Next, the researchers showed that scratching causes pain-sensing neurons to release a compound called substance P. In turn, substance P activates mast cells, which are key coordinators of inflammation that drive itchiness and inflammation via recruitment of neutrophils.

“In contact dermatitis, mast cells are directly activated by allergens, which drives minor inflammation and itchiness,” explained Kaplan. “In response to scratching, the release of substance P activates mast cells through a second pathway, so the reason that scratching triggers more inflammation in the skin is because mast cells have been synergistically activated through two pathways.”

Mast cells are culprits in a range of inflammatory skin conditions and allergic reactions, but they’re also important for protecting against bacteria and other pathogens. As such, the researchers wondered if scratching-induced activation of mast cells could affect the skin microbiome.

In experiments led by coauthor Marlies Meisel, Ph.D., assistant professor of immunology at Pitt, the team showed that scratching reduced the amount of Staphylococcus aureus, the most common bacteria involved in skin infections, on the skin.

“The finding that scratching improves defense against Staphylococcus aureus suggests that it could be beneficial in some contexts,” said Kaplan. “But the damage that scratching does to the skin probably outweighs this benefit when itching is chronic.”

Now, the researchers are investigating new therapies for dermatitis and other inflammatory skin conditions such as rosacea and urticaria that suppress inflammation by targeting receptors on mast cells.

Other researchers on the study were Youran Zhang, Chien-Sin Chen, Ph.D., Tara N. Edwards, Ph.D., Torben Ramcke, M.D., Lindsay M. McKendrick, Eric S. Weiss, Jacob E. Gillis, Colin R. Laughlin, Simran K. Randhawa, Catherine M. Phelps, Kazuo Kurihara, M.D., Ph.D., Hannah M. Kang, Sydney-Lam N. Nguyen, Jiwon Kim, Tayler D. Sheahan, Ph.D., Sarah E. Ross, Ph.D., and Tina L. Sumpter, Ph.D., all of Pitt and UPMC; and Sumeyye Ozyaman, of Pitt and Istanbul Medipol University.

This research was supported by the National Institutes of Health (T32NS73548, T32CA0820840, R01DK130897, U24EY035102, K99NS126569, R01AR071720 and R01AR077341) and the German Research Foundation.

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Journal

Science

DOI

10.1126/science.adn9390 

Article Title

Scratching promotes allergic inflammation and host defense via neurogenic mast cell activation

Most engineered human cells created for studying disease

...BUT NOT ALL!

Researchers have engineered and analyzed many random versions of human genomes in cell lines to ultimately understand the role of structural changes in disease

Wellcome Trust Sanger Institute

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The most complex engineering of human cell lines ever has been achieved by scientists, revealing that our genomes are more resilient to significant structural changes than was previously thought.

Researchers from the Wellcome Sanger Institute, Imperial College London, Harvard University in the US and their collaborators used CRISPR prime editing to create multiple versions of human genomes in cell lines, each with different structural changes. Using genome sequencing, they were able to analyse the genetic effects of these structural variations on cell survival.

The research, published today (30 January) in Science, shows that as long as essential genes remain intact, our genomes can tolerate significant structural changes, including large deletions of the genetic code. The work opens the door to studying and predicting the role of structural variation in disease.

Structural variation is a change in the structure of an organism’s genome, such as deletions, duplications and inversions of the genetic sequence. These structural changes to the genome can be significant, sometimes affecting hundreds to many thousands of nucleotides – the basic building blocks of DNA and RNA.

Structural variants are associated with developmental diseases and cancer. However, our ability to study the effects of structural variation in the genomes of mammals, and the role they play in disease, has been difficult due to the inability to engineer these genetic changes.

To overcome this challenge, Sanger Institute researchers and their collaborators set out to develop new approaches for creating and studying structural variation.

In a new study, the team used a combination of CRISPR prime editing1 and human cell lines2 – groups of human cells in a dish – to generate thousands of structural variants in human genomes within a single experiment.

To do this, researchers used prime editing to insert a recognition sequence into the genomes of the human cell lines to target with recombinase3 – an enzyme that enabled the team to ‘shuffle’ the genome. By inserting these recombinase handles into repetitive sequences, which are hundreds and thousands of identical sequences in the genome, with a single prime editor they were able to integrate up to almost 1,700 recombinase recognition sites into each cell line. This resulted in more than 100 random large-scale genetic structural changes per cell. This is the first time that it’s been possible to ‘shuffle’ a mammalian genome, especially at this scale.

The team then studied the impacts of the structural variation on the human cell lines. Using genomic sequencing, the team was able to take ‘snapshots’ of the human cells and their ‘shuffled’ genomes over the course of a few weeks, watching which cells survived and which died.

As expected, they found that when structural variation deleted essential genes, this was heavily selected against and the cells died. However, they found that groups of cells with large-scale deletions in the genomes that avoided essential genes, survived.

The team also conducted RNA sequencing of the human cell lines, which measures gene activity, known as gene expression. This revealed that large-scale deletions of the genetic code, especially in non-coding regions, did not seem to impact the gene expression of the rest of the cell.

The researchers suggest that human genomes are extremely tolerant of structural variation, including variants that change the position of hundreds of genes, as long as essential genes are not deleted4. Plus, they query whether much of the non-coding DNA in human genomes is dispensable, but further research that engineers additional deletions in more cell lines is needed.

In a related paper, also published today in Science5, researchers from the University of Washington had a similar goal of creating structural variants at large scale and studying their effects on the human genome. This team used a different approach, adding recombinase sites to transposons – mobile genetic elements – that randomly integrated in the genomes of human cell lines and mouse embryonic stem cells.

Using their method, they demonstrated that the effects of the induced structural variants can be read out using single-cell RNA sequencing. This advance paves the way for large screens of structural variant impact, potentially improving the classification of structural variants found in human genomes as benign or clinically significant. Both studies came to similar conclusions that human genomes are surprisingly tolerant to some substantial structural changes, although the full extent of this tolerance remains to be explored in future studies enabled by these technologies.

Overall, this research presents the most engineered human cell lines to date. For the first time, researchers are able to create structural variants in human genomes, at large scales in a single experiment, and analyse the many random versions of our genomes.

This work will increase our understanding of the role of structure variants in disease, which may eventually lead to predictions being made around how damaging structural variants could be in an individual. This research also helps narrow the range of the genome for exploring structural variation that leads to disease, especially if non-coding DNA can be discounted.

Plus with this new tool, scientists can generate new, streamlined cell lines with evolved properties, such as being optimised for growth, studying drug resistance, or bioengineered to create medicines.

Dr Jonas Koeppel, co-first author previously at the Wellcome Sanger Institute, and now at the University of Washington, said: “If the genome was a book, you could think of a single nucleotide variant as a typo, whereas a structural variant is like ripping out a whole page. These structural variants are known to play roles in developmental diseases and cancer, but it has been difficult to study them experimentally. Through creative and collaborative thinking, we’ve been able to do complex engineering in human cells that no-one has done before. By shuffling the genomes of human cell lines at large scale, we’ve shown that our genomes are flexible enough to tolerate significant structural changes. These tools will help focus future studies into structural variations and their roles in disease.”

Dr Raphael Ferreira, co-first author and a postdoctoral researcher in the Church Lab at Harvard Medical School, said: “Our studies were only made possible because the right mix of ingredients came together at the right time: the scale of genome sequencing, cutting-edge genome engineering, and the use of recombinases. And importantly, the open and collaborative nature of our science across global borders. Our teams independently had similar ideas and came together to make these pioneering studies happen.”

Professor Tom Ellis, an author of the study and Associate Faculty at the Wellcome Sanger Institute, based at the Department of Bioengineering at Imperial College London, said: “Ten years ago, people thought it would take decades of work and hundreds of millions of dollars to engineer a rearrangeable human genome that scientists could use to study genome structure, but this work shows a way to make this possible right now. It's exciting to think about what new biology we can learn from rearrangeable genomes and where this might go next.”

Dr Leopold Parts, co-lead author at the Wellcome Sanger Institute, said: “These studies represent a step change in the parallel creation and evaluation of structural variation in human genomes. The tools to create a single variant at a time had been available for decades, but we have demonstrated that interrogating variants and making randomised human genomes at scale is now doable. This gives new entry points both into the study of disease-associated variation, as well as opportunities for bioengineering.”

ENDS

Contact details:
Emily Mobley

Press Office
Wellcome Sanger Institute
Cambridge, CB10 1SA
Email: press.office@sanger.ac.uk

Notes to Editors:

1. For more information on prime editing, read our blog: https://sangerinstitute.blog/2023/07/17/prime-editing-explainer/ 
2. The human cell lines used in this study are HEK293T, which is specialised for genome engineering, and HAP1, which includes just one copy of the genome, meaning that subtle changes caused by structural variants are clearer to see. These cells do not have the ability to make an organ or tissue. They are groups of separate cells growing in a dish that are simply tools used to understand the human genome.
3. Recombinases are enzymes that catalyse site-specific recombination events within DNA.
4. The researchers note the caveat that these results are from experiments done in cultured human cells in a dish, and may not truly reflect the situation in a living organism.
5. Sudarshan Pinglay et al. (2025) ‘Multiplex generation and single cell analysis of structural variants in mammalian genomes.’ Science. DOI: 10.1126.science.ado5978

Publication:
Jonas Koeppel et al. (2025) ‘Randomizing the human genome by engineering recombination between repeat elements.’ Science. DOI: 10.1126/science.ado3979

Funding:
This research was supported by Wellcome and others. Full details can be found in the publication.

Selected websites:

About Imperial College London
We are Imperial [imperial.ac.uk] – a world-leading university for science, technology, engineering, medicine and business (STEMB), where scientific imagination leads to world-changing impact.

As a global top ten university in London, we use science to try to understand more of the universe and improve the lives of more people in it. Across our nine campuses and throughout our Imperial Global network, our 22,000 students, 8,000 staff, and partners work together on scientific discovery, innovation and entrepreneurship. Their work navigates some of the world’s toughest challenges in global health, climate change, AI, business leadership and more.

Founded in 1907, Imperial’s future builds on a distinguished past, having pioneered penicillin, holography and fibre optics. Today, Imperial combines exceptional teaching, world-class facilities and a habit of interdisciplinary practice to unlock scientific imagination.

The Wellcome Sanger Institute
The Wellcome Sanger Institute is a world leader in genomics research. We apply and explore genomic technologies at scale to advance understanding of biology and improve health. Making discoveries not easily made elsewhere, our research delivers insights across health, disease, evolution and pathogen biology. We are open and collaborative; our data, results, tools, technologies and training are freely shared across the globe to advance science.

Funded by Wellcome, we have the freedom to think long-term and push the boundaries of genomics. We take on the challenges of applying our research to the real world, where we aim to bring benefit to people and society.

Find out more at www.sanger.ac.uk or follow us on Twitter, Instagram, Facebook, LinkedIn and on our Blog.

About Wellcome
Wellcome supports science to solve the urgent health challenges facing everyone. We support discovery research into life, health and wellbeing, and we’re taking on three worldwide health challenges: mental health, infectious disease and climate and health. https://wellcome.org/

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Journal

Science

DOI

10.1126/science.ado3979 

Article Title

Randomizing the human genome by engineering recombination between repeat elements

Article Publication Date

31-Jan-2025

 

Polar bear energetic model reveals drivers of polar bear population decline

Summary author: Walter Beckwith

American Association for the Advancement of Science (AAAS)

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Polar bears in Western Hudson Bay have seen their population nearly halved over the last several decades, largely due to dwindling sea ice and limited hunting opportunities, according to the findings of a novel bioenergetic model using data spanning more than 40 years. The findings reveal the relationship between bears’ individual energy needs and environmental limitations in driving population trends, highlighting energy as the central limiting factor behind the decline of a key Arctic apex predator. The Arctic is warming faster than any other region on Earth, leading to significant sea ice loss, ecosystem transformations, and heightened threats to ice-dependent species like polar bears (Ursus maritimus). These animals rely on sea ice to hunt seals, their primary food source, but as ice melts during warmer months, they are forced onto land or into less productive waters, relying on stored energy reserves due to the lack of adequate food sources. Food deprivation caused by changes in seasonal sea ice has been linked to declines in polar bear populations. However, conservation efforts are limited by a lack of data for most polar bear subpopulations and a framework to understand how sea ice loss affects the animals throughout their lives. To investigate the relationship between declining sea ice and polar bear populations, Louise Archer and colleagues compiled population monitoring and capture data collected from polar bears in Western Hudson Bay, Canada, over the last 42 years and developed an individual-based bioenergetic model. The model, grounded in physiological principles, integrates energy acquisition and expenditure – such as feeding, body maintenance, movement, growth, and reproduction – into a unified energy budget spanning an individual bear’s life cycle. The findings show that sea ice loss and resultant feeding limitations were the primary drivers of a ~50% population decline since the mid-1990s, demonstrating how individual energetic constraints shape population-level outcomes. What’s more, Archer et al. note that this framework, although developed for polar bears, is adaptable to other species facing constraints on foraging or energy use due to environmental or human-driven changes, offering broad utility in addressing global change impacts and informing conservation and policy decisions.

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Journal

Science

DOI

10.1126/science.adp3752 

Article Title

Energetic constraints drive the decline of a sentinel polar bear population

Article Publication Date

31-Jan-2025

Polar bear population decline the direct result of extended ‘energy deficit’ due to lack of food

Study finds polar bears are struggling to get enough to eat in face of dwindling sea ice due to climate change

University of Toronto

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Researcher Louise Archer.

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Credit: Handcraft Creative

U of T Scarborough researchers have directly linked population decline in polar bears living in Western Hudson Bay to shrinking sea ice caused by climate change.

The researchers developed a model that finds population decline is the result of the bears not getting enough energy, and that’s due to a lack of food caused by shorter hunting seasons on dwindling sea ice.

“A loss of sea ice means bears spend less time hunting seals and more time fasting on land,” says Louise Archer, a U of T Scarborough postdoc and lead author of the study.

“This negatively affects the bears’ energy balance, leading to reduced reproduction, cub survival and, ultimately, population decline.”

The “bio-energetic” model developed by the researchers tracks the amount of energy the bears are currently getting from hunting seals and the amount of energy they need in order to grow and reproduce. What’s unique about the model is that it follows the full lifecycle of individual polar bears — from cub to adulthood — and compares it to four decades of monitoring data from the Western Hudson Bay polar bear population between 1979 and 2021.

During this period, the polar bear population in this region has declined by nearly 50 per cent. The monitoring data shows the average size of polar bears is also in decline. The body mass of adult females has dropped by 39kg (86lbs) and one-year-old cubs by 26kg (47lbs) over a 37-year period.

The researchers’ model provides a close match to the monitoring data, meaning it provides an accurate assessment of what is happening and will continue to happen to the polar bear population if it keeps experiencing sea ice loss and a greater amount of time in energy deficit.

“Our model goes one step further than saying there’s a correlation between declining sea ice and population decline,” says Péter Molnár, an associate professor in the Department of Biological Sciences at U of T Scarborough and co-author of the study.

“It provides a mechanism that shows what happens when there is less ice, less feeding time and less energy overall. When we run the numbers, we get a near one-to-one match to what we’re seeing in real life.”

Polar bear mom and cubs particularly vulnerable

The researchers, which include co-authors from Environment and Climate Change Canada, noted that cubs face the brunt of these climate-induced challenges.

Archer says that shorter hunting periods result in mothers producing less milk, which jeopardizes cub survival. The cubs face reduced survival rates during their first fasting period if they fail to gain enough weight.

Mothers are also having fewer cubs. Monitoring data shows cub litter sizes have dropped 11 per cent compared to almost 40 years ago, and mothers are keeping their cubs longer because they aren’t strong enough to live on their own.

“It’s pretty simple — the survival of cubs directly impacts the survival of the population,” says Archer, whose research is funded through a Mitacs Elevate postdoctoral fellowship and the non-profit organization Polar Bears International.

Broader applications for the model

Western Hudson Bay has long been considered a bellwether for polar bear populations globally, and as the Arctic warms at a rate four times faster than the global average, the researchers warn of similar declines in other polar bear populations.

“This is one of the southernmost populations of polar bears, and it’s been monitored for a long time, so we have very good data to work with,” says Molnár, who is an expert on how global warming impacts large mammals.

“There’s every reason to believe what is happening to polar bears in this region will also happen to polar bears in other regions, based on projected sea ice loss trajectories. This model basically describes their future.”

The study, which is published in the journal Science, received funding from the Natural Sciences and Engineering Research Council of Canada and the Canada Foundation for Innovation.

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Journal

Science

DOI

10.1126/science.adp3752 

Article Title

Energetic constraints drive the decline of a sentinel polar bear population

Article Publication Date

30-Jan-2025

 DOLLY & 23ANDME.COM

Ancient DNA analyses bring to life the 11,000-year intertwined genomic history of sheep and humans

Trinity College Dublin

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Vessel supported by two rams, 2600 to 2500 BCE, object number 1989.281.3, Gift of Norbert Shcimmel Trust, 1989, open access Met Museum.

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Credit: Gift of Norbert Shcimmel Trust, 1989, open access Met Museum.

Sheep have been intertwined with human livelihoods for over 11,000 years. As well as meat, their domestication led to humans being nourished by their protein-rich milk and clothed by warm, water-resistant fabrics made from their wool. 

Now, an international and interdisciplinary team of researchers led by geneticists from Trinity College Dublin and zooarchaeologists from LMU Munich and the Bavarian State Collections of Natural History (SNSB) has deciphered the prehistoric cultural trajectory of this species by analysing 118 genomes recovered from archaeological bones dating across 12 millennia and stretching from Mongolia to Ireland. 

The earliest sheep-herding village in the sample, Aşıklı Höyük in central Türkiye, has genomes that seem ancestral to later populations in the wider region, confirming an origin in captures of wild mouflon over 11,000 years ago in the western part of the northern Fertile Crescent.

By 8,000 years ago, in the earliest European sheep populations, the team found evidence that farmers were deliberately selecting their flocks – in particular for the genes coding for coat colour.  Along with a similar signal in goats, this is the earliest evidence for human moulding of another animal’s biology and shows that early herders, like today’s farmers, were interested in the beautiful and unusual in their animals.

Specifically, the main gene the team found evidence of selection near was one known as “KIT”, which is associated with white coat colour in a range of livestock.

Also by that time, the earliest domestic sheep genomes from Europe and further east in Iran and Central Asia had diverged from each other. However, this separation did not last as people translocated sheep from eastern populations to the west.  

First, in parallel with human cultural influences spreading out from the early cities of Mesopotamia we see sheep genomes moving west within the Fertile Crescent around 7,000 years ago.

Second, the rise of pastoralist peoples in the Eurasian steppes and their westward spread some 5,000 years ago profoundly transformed ancestral European human populations and their culture. This process changed the makeup of human populations, for example, altering the ancestry of British peoples by around 90%, and introduced the Indo-European language ancestor of the tongues spoken across the continent today.

From the dataset used in this study it now seems that this massive migration was fuelled by sheep herding and exploitation of lifetime products, including milk and probably cheese, as it is around the same time that sheep ancestries are also changed. Consequently, by the Bronze Age, herds had about half their ancestry from a source in the Eurasian steppe.

Dr Kevin Daly, Ad Astra Assistant Professor at UCD School of Agriculture and Food Science and an Adjunct Assistant Professor in Trinity’s School of Genetics and Microbiology, is the first author on the research article that has just been published in leading international journal Science. He said: “One of our most striking discoveries was a major prehistoric sheep migration from the Eurasian steppes into Europe during the Bronze Age. This parallels what we know about human migrations during the same period, suggesting that when people moved, they brought their flocks with them.”

Dan Bradley, leader of the research and Professor of Population Genetics in Trinity’s School of Genetics and Microbiology, said: “This research demonstrates how the relationship between humans and sheep has evolved over millennia. From the early days of domestication through to the development of wool as a crucial textile resource, sheep have played a vital role in human cultural and economic development.”

Joris Peters, co-corresponding author, Professor of Paleoanatomy, Domestication Research and the History of Veterinary Medicine at LMU Munich and Director of the State Collection for Paleoanatomy Munich (SNSB-SPM), said: “Our study, while convincingly reconciling morphological and genomic evidence of the geographic origin of domestic sheep, clearly illustrates that further transdisciplinary research is needed to clarify the patterns of dispersal and selection of the many landraces occurring today in Eurasia and Africa.”

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DOI

10.1126/science.adn2094 

Scottish Blackface from Applecross, Scotland - a common sheep breed of the British Isles. This breed is represented in the panel of modern reference genomes.

Credit

J. Peters, LMU/SNSB

Today's descendants of the first domestic sheep of Central Anatolia. 

Credit

N. Pollath, SNSB.

Journal

Science