Human gut bacteria genome is directly impacted by industrialization

Phylogenetic methods built to trace evolution over billions of years find that gut bacteria in industrialized societies have more and different genes, which might influence human health

Okinawa Institute of Science and Technology (OIST) Graduate University

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From regulating our metabolism and immune defense to influencing our hormonal and neurological pathways via the gut-brain axis, our gut microbiome has been found to serve more and more roles pivotal to our health.

The bacteria in our guts inhabit very different worlds depending on how we live. Diet, sanitation and medication all differ between industrialized and non-industrialized societies, and we have known for some time that these factors change which bacteria are present. But do our symbiotic bacteria evolve in response to our evolving lifestyle?

A new study published in Cell has now shown that the answer appears to be yes, and in parallel across different species of bacteria, finding that strains from industrialized hosts carry more genes, which were gained recently, mostly from other microbes. The study also found signs of selection in the same kinds of functions across different species, including stress response, remodeling of the cell envelope, and central metabolism. These include genes for making vitamin B12, and genes for making lipopolysaccharide, a component of the bacterial surface that our immune system recognizes, which may have consequences for human health that remain to be explored.

The study was led by researchers from Kiel University and MIT, with evolutionary modelling by researchers from the Model-Based Evolutionary Genomics Unit at the Okinawa Institute of Science and Technology (OIST), headed by Professor Gergely Szöllősi.

“It's always exciting when the methods and tools we develop to answer deep evolutionary questions can be repurposed to datasets and questions closer to the present that may have a more direct impact on our everyday life. Understanding how the bugs in our guts pick up new genes is a good example for this. I hope our results will inspire further studies to use this knowledge in supporting us to live a healthier life in our changing environment,” says Lénárd Szánthó, a senior bioinformatician in the OIST unit.

From deep past to modern history

The multinational team focused on ten bacterial species that were well-sampled in both industrialized and non-industrialized hosts. In all ten, strains from industrialized hosts had larger sets of protein-coding genes, a difference that was statistically significant in eight, and strains within a species differed more from one another in gene content.

Larger genomes could mean two very different things. The strains may have gained the genes recently, or their ancestors may already have had them, and industrial environments simply favored those strains. Telling these explanations apart is where the OIST contribution comes in. Phylogenetic reconciliation compares the family tree of each gene with the family tree of the species that carries it, and any mismatches between the trees reveal where genes were gained, lost, or transferred. The OIST group developed these methods to study the deep past, including the early evolution of bacteria and the origin of fungi, on time scales of hundreds of millions and billions of years. Now, Szánthó has modified them to the relatively recent history of the gut microbiome as it adapts to industrialization.

The results were clear: gene gains were concentrated on the tips of the trees (i.e. in recent evolution) and were higher along branches associated with industrialized hosts. Between 80% and 90% of the gains were horizontal gene transfers, in which bacteria take up genes from other microbes rather than inheriting them from their parents, often together with mobile elements such as plasmids and phages.

"These methods were built to look back hundreds of millions and billions of years, so it was not obvious that they would tell us anything about something this recent," said Szöllősi. "Lénárd made them work for this problem, and the picture that comes out is that bacteria in industrialized hosts have been acquiring genes from their neighbors recently, and this is what makes their genomes larger."

The authors are careful about what the data cannot show. It is still unclear which aspect of industrial life, whether diet, medication, sanitation, or something else, is responsible for these patterns. It is also not settled that the larger genomes are themselves an adaptation, since they may partly reflect weaker selection against extra genes. And the analysis covers ten species, so whether the patterns hold more widely will need further work.

The team worked with cultured bacteria as well as with DNA reconstructed from stool samples. They added 1,841 new genomes to the collection of the Global Microbiome Conservancy, and used a further 4,140 data samples from the collection for a total of 5,981 isolate genomes from 56 donors in 9 countries. The Global Microbiome Conservancy is an international initiative that works with communities around the world, with a particular emphasis on populations underrepresented in microbiome research, and is building an open, non-profit library of human gut bacteria.

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Journal

Cell

DOI

10.1016/j.cell.2026.10.014

Method of Research

Data/statistical analysis

Subject of Research

Cells

Article Title

Convergent genomic evolution of human gut bacteria along an industrialization gradient

Article Publication Date

2-Nov-2026

COI Statement

R.J.X. is a co-founder of Convergence Bio, a board director at MoonLake Immunotherapeutics, a consultant to Nestlé, and a member of the advisory boards at Magnet Biomedicine and Arena Bioworks. None of the organizations listed above provided funding for this study.

 

Bacteria DNA has evolved to withstand copper

Copper-based coatings are often used to slow bacterial growth on marine surfaces — but bacteria have adapted

American Institute of Physics

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image: 

Coated and uncoated PVC panels (top), which encountered bacterial growth after being placed in the Chesapeake Bay (bottom, left). The bacteria were then assayed and their genetics studied (bottom, center and right).

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Credit: Kenan P. Fears

WASHINGTON, Oct. 13, 2026 — Marine bacteria have evolved to bypass the copper-based coatings placed under ships to stop the growth of barnacles, algae, and other marine life. This necessitates new methods for managing biofouling — the unwanted accumulation of marine organisms — on ship hulls.

In Biointerphases, an AVS journal published by AIP Publishing, researchers from the U.S. Naval Research Laboratory and Duke University studied the genetic characteristics of various bacteria species responsible for their survival on copper surfaces, a step toward inhibiting these copper-resistant genes.

“We have observed increasing copper resistance in some of the ports our team frequents over the past decade, particularly in ports with heavy tourist [or] industry shipping activity,” said author Kenan Fears. “We wanted to identify the resistance pathways across a diverse microbial community to provide insight into how members of a complex community could be acting symbiotically to resist toxic environments.”

The researchers placed pieces of PVC panels in the Chesapeake Bay, some coated with a copper-based coating and some left uncoated. After two weeks, they extracted the DNA and sequenced the genomes of the bacterial colonies that grew on the panels to identify the copper-resistant genes and tested each colony’s tolerance against copper-based water treatments.

Surprisingly, the bacteria species had a lot in common regardless of whether they grew near the copper-based coating. The bacteria from the control colonies — the ones that did not initially grow on the copper-coated surfaces — were just as copper-resistant and could thrive at copper concentrations above 70 milligrams per liter.

“To put that in perspective, the U.S. Environmental Protection Agency limit in seawater for a short-term spike in copper is 18 micrograms per liter,” Fears said.

This is a likely marker of evolution and bacteria adapting to their new environments.

“Copper was not always in a water-soluble state; it only became so after oxygen accumulated in Earth’s atmosphere,” Fears said. “However, as environmental copper loading has increased, the bacteria with the best defense mechanisms continued to reproduce.”

The researchers hope to use their findings to target the molecular pathways that help bacteria express copper-resistant genes, weakening their ability to survive in copper-rich environments.

“Our research suggests the smarter path moving forward is to design antifouling coatings that select microbial communities that either help deter macrofouler settlement — like barnacles or tubeworms — or do not impede the release of biocidal compounds,” Fears said. “With increasing regulatory pressure on copper use in antifouling coatings, there is an urgent need for alternatives.”

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The article “Extreme copper tolerance and genomic adaptation in early-stage marine biofilms” is authored by Kailey N. Richard, Sara M. Tuck, Sophie M. Colston, Maryssa A. Beasley, W. Judson Hervey, Kevin Le, Sean Brown, Katherine J. Franz, and Kenan P. Fears. It will appear in Biointerphases on Oct. 13, 2026 (DOI: 10.1116/6.0005640). After that date, it can be accessed at https://doi.org/10.1116/6.0005640.

ABOUT THE JOURNAL

Biointerphases, an AVS journal published by AIP Publishing, emphasizes quantitative characterization of biomaterials and biological interfaces. As an interdisciplinary journal, a strong foundation of chemistry, physics, biology, engineering, theory, and/or modelling is incorporated into originated articles, reviews, and opinionated essays. See https://pubs.aip.org/avs/bip.

ABOUT AVS

AVS is an interdisciplinary, professional society with some 4,500 members worldwide. Founded in 1953, AVS hosts local and international meetings, publishes five journals, serves members through awards, training and career services programs, and supports networking among academic, industrial, government, and consulting professionals. Its members come from across the fields of chemistry, physics, biology, mathematics, engineering, and business and share a common interest in basic science, technology development and commercialization related to materials, interfaces, and processing.

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Journal

Biointerphases

DOI

10.1116/6.0005640

Article Title

Extreme copper tolerance and genomic adaptation in early-stage marine biofilms

Article Publication Date

13-Oct-2026

Newly discovered antiviral system in bacteria is ‘strangest of its kind’

The complex Rube Goldberg-like molecular machinery could inspire novel technology to study and treat disease

Gladstone Institutes

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Gladstone scientists, including Karen Zhang, uncovered a counterintuitive class of bacterial defense systems, known as type VI retrons, that can be adapted to engineer more efficient gene editing tools.

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Credit: Michael Short/Gladstone Institutes

SAN FRANCISCO—Researchers at Gladstone Institutes have uncovered an extraordinarily unusual bacterial immune system that operates in reverse of known defenses.

The discovery, published in Molecular Cell, details the mechanics of "type VI retrons"—a uniquely counterintuitive class of bacterial defenses. More than just a biological curiosity, decoding these complex systems provides a molecular blueprint that scientists can adapt to engineer more efficient DNA-editing tools for human health and therapies.

“This is, by far, the strangest of the retron systems that we or anyone else has come across,” says Gladstone Investigator Seth Shipman, PhD, senior author of the new study. “These retrons operate with Rube Goldberg-level complexity, using molecular mechanisms that we would never have thought to invent, but that we’ll use in future technologies.”

Bacteria have long evolved specialized defenses to destroy phages, which are viruses that target bacterial cells. A particularly powerful line of defense, known as retrons, recognize viral attacks and trigger self-destruction to protect the broader bacterial colony.

Because retrons can also efficiently modify and deliver single-stranded DNA, researchers including Shipman and his team are working to harness them to rewrite disease-causing mutations inside human cells with unprecedented precision.

Inverted Expectations

Many types of retron systems exist, but they all follow the same basic principle: they sense when a specific strain of phage has attacked the bacterial cell, and they then unleash a toxic protein to kill the cell. This self-destruction stops the phage before it has a chance to multiply and spread to neighboring cells in the same colony.

Decades of research have led to the general understanding that all retrons produce a toxin that, in uninfected cells, is constantly present but deliberately repressed by small, single-stranded DNA molecules. When a phage invades, it perturbs the DNA and causes it to release the toxin.

“The way we typically detect retrons inside uninfected cells is by looking for this single-stranded DNA,” says Karen Zhang, a PhD student in Shipman’s lab and lead author of the study. “But type VI retrons caught our attention because they didn’t appear to have this signature. It was very odd, and we wondered if they might be broken.”

But when the scientists tested certain bacteria containing type VI retrons, they found that the retrons were still able to successfully defend their cells against phages.

“That kicked off a long molecular odyssey,” Shipman says. “Whenever we tried the experiments we normally use to study retrons, they would fail, so we kept having to think of new ways to figure out how these retrons work.”

The experimental saga ultimately revealed that, unlike other retrons, type VI retrons do not produce noticeable levels of single-stranded DNA nor toxin in uninfected cells. Instead, the entry of a phage into a cell is needed to trigger the retron to start producing single-stranded DNA.

Once it builds up, the DNA then interacts with an RNA that has been blocking production of the toxin. This interaction releases the block, allowing toxin production to ramp up.

The toxin appears to be a tiny protein that embeds itself into the membrane surrounding the cell, which destabilizes the cells and kills it.

“It’s almost the mirror-image version of how we traditionally view retrons, because the DNA switches on toxin production instead of inhibiting an already-produced toxin,” Zhang says. “It would be fascinating to explore how bacterial evolution could have resulted in such a complex molecular system—whether type VI retrons are older or newer than other retrons, or whether they’re a stepping stone between different types.”

Rethinking Retron Research

To decipher the unique machinery of type VI retrons, the team had to concoct novel experiments and repurpose existing methods in new ways. One early breakthrough, for instance, arose from the repeated, mysterious failure of standard methods to detect DNA made by type VI retrons in uninfected cells.

The researchers turned to a different tool called Spacer-seq previously developed in Shipman’s lab. This tool harnesses the molecular components of another kind of bacterial immune system, CRISPR-Cas, to create a record of gene activity inside a cell.

“We had just about given up hope that any DNA was being made when this approach finally revealed a very, very low level of production in uninfected cells,” Zhang says.

The finding motivated the team to keep digging, and further experiments showed that the DNA only ramps up to defensive levels after the phage enters.

Nature-Inspired Tools and Treatments

The unique machinery of type VI retrons is already inspiring the development of novel tools in Shipman’s lab, including new synthetic sensors and switches that can control gene activity.

“This system represents a unique way to potentially build a molecular sensor and switch encoded in DNA and RNA, that no one has thought of before,” Zhang says. “Synthetic sensors and switches have many possible applications, both in treating disease and in designing experiments to better understand how certain diseases operate.”

The tiny, highly potent toxins produced by the type VI retrons could also prove useful in a medical context. The scientists are working on ways to incorporate these toxins into new types of antimicrobial therapies, which could target and kill bacteria that cause human disease.

“This study highlights why it’s so important for a molecular technology development lab like ours to keep looking to nature for inspiration,” Shipman says. “We can use what evolution has given us as starting points to build complex machines that would have been tremendously hard to even conceptualize.”

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About the Study

The study, “Reverse transcribed ssDNA derepresses translation of a retron antiviral protein,” was published in Molecular Cell on October 13, 2026. In addition to Shipman and Zhang, authors are Matías Rojas-Montero, Darshini Poola, and Alejandro González-Delgado of Gladstone; Josepha Klas, Arturo Carabias, Dennis Zhang, Mario Mestre, Ruiliang Zhao, Ana Dávila-Hidalgo, Guillermo Montoya, and Rafael Pinilla-Redondo of the University of Copenhagen; and Lieza Chan and Kliment Verba of UC San Francisco.

The work was supported by the National Science Foundation, the Robert J. Kleeberg Jr. and Helen C. Kleberg Foundation, the Gordon and Betty Moore Foundation, the Lundbeck Foundation, the Fulbright U.S. Student Program, the Junta de Castilla y León and European Social Fund Plus, the European Molecular Biology Organization, the Novo Nordisk Foundation, the European Research Council, and the Villum Foundation.

About Gladstone Institutes

Gladstone Institutes is an independent, nonprofit life science research organization that uses visionary science and technology to overcome disease. Established in 1979, it is located in the epicenter of biomedical and technological innovation, in the Mission Bay neighborhood of San Francisco. Gladstone has created a research model that disrupts how science is done, funds big ideas, and attracts the brightest minds.

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Journal

Molecular Cell

DOI

10.1016/j.molcel.2026.09.026

Article Title

Reverse transcribed ssDNA derepresses translation of a retron antiviral protein

Article Publication Date

13-Oct-2026

 

New tool closes gap on untapped potential of phages

University of Otago

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A new tool to mutate bacteriophages – viruses that infect bacteria – provides a “big leap” forward in both our understanding of how they function, and our ability to harness their full potential.

Developed by researchers in the University of Otago – Ōtākou Whakaihu Waka, New Zealand, Department of Microbiology and Immunology, the method features on the latest cover of prestigious international journal Nature Microbiology.

Senior author Professor Peter Fineran says bacteriophages, or simply phages, have “huge potential” to combat the antimicrobial resistance crisis, and for increasing sustainable agriculture as an alternative to agrochemicals, because they can destroy bacteria.  

“But our knowledge of phages is probably like the understanding of antibiotics back in the 1950s. Many phage genes are currently in the area of microbial dark matter – encoding functions we just don’t understand – which is limiting our ability to use phages in healthcare and biotechnology.

“This new development is a big leap in how we can rapidly understand phage biology and then use that knowledge to make phages work better to help achieve our goals.” 

Co-lead author Dr Manuela Fuchs says the new method allows for genome-wide mutagenesis of bacteriophages using CRISPR-Cas technology.

The researchers utilised transposon insertion sequencing – using a mobile piece of DNA which can jump in and disrupt a gene – combined with CRISPR-anti-CRISPR-based selection, to select phages that have been mutated. This allows them to identify genes that are essential and genes that are non-essential for phage survival.

“Once we had that established, we thought we could expand the technique and also use it to add genes directly into the phage genomes. We essentially found it is possible to load additional genes on that transposon, not just our anti-CRISPR protein. While we added a fluorescent marker, it could be used to, for example, add additional anti-defence genes to phages, to improve their therapeutic potential,” Dr Fuchs says.

Senior author Dr Leah Smith says the method enables genes to be automatically inserted somewhere while maintaining phage function.

“This is a systematic, broadly applicable, and cost-effective way to not only investigate gene function, but also rapidly engineer phage genomes.

“This opens up new opportunities for both fundamental research and future therapeutic development.”

One particular example of this would be biofilms, which can cause hard-to-treat infections on prosthesis implants and medical devices.

“With this new technique, we could quickly load phages to have more things that stop some bacterial defences so that they can be harnessed to kill pathogens more easily,” Dr Smith says.

Funding: 

This research was supported by Professor Fineran’s Royal Society of New Zealand – Te Apārangi James Cook Research Fellowship, Dr Smith’s Royal Society Marsden Fund grant and L’Oréal-UNESCO For Women in Science Fellowship, Dr Fuchs’ Feodor Lynen Research Fellowship from the Alexander von Humboldt Stiftung, and Natalie Kyte’s University of Otago Doctoral Scholarship.
 

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Journal

Nature Microbiology

DOI

10.1038/s41564-026-02486-1

Article Title

Defining the essential genome of diverse phages with phage Tn-seq

Article Publication Date

25-Sep-2026

 

First-of-its-kind preventative phage therapy provides promising results

Virginia Tech

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(From left) Roger Bataglioli and Hiba Baaziz in the lab.

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Credit: Photo by Felicia Spencer for Virginia Tech.

The mammalian gut microbiome is teeming with a delicate balance of bacteria and the viruses that keep them in check, called bacteriophages, or phages. Each bacterial species usually has its own set of phage partners. 

When bad bacteria enter this ecosystem, there are typically no phages present, allowing them to cause mayhem. By the time the host is sick, it is too late for phages; they’ll simply reach a balance with the bad bacteria.

But what if the phages in the gut could prepare for the orally ingested pathogen and strike it down as it enters the gut, negating the need for a battle?

Associate Professor and Blackwood Junior Faculty Fellow Bryan Hsu and his team recently demonstrated that this prophylactic approach, using an engineered nonpathogenic E. coli bacterium, successfully protected mice from an oral salmonella infection. Their work was published in Nature Microbiology.

The team believes this is a step toward an additional weapon against illnesses. 

“Eventually, in the future, this could be used to treat other diseases,” said Rogerio A. Bataglioli, a postdoctoral fellow in the Department of Biological Sciences and lead author of the study. “It’s not about replacing antibiotics but having one more option on the shelf to fight infections.” 

Bacteriophages, or phages, are viruses of bacteria and do not infect humans or animals. Hsu said phage therapy, the use of phages to treat bacterial infections, is particularly hard to make successful for treating intestinal pathogens. 

“It’s challenging, especially in the gut, because phages and bacteria tend to coexist for long periods of time,” said Hsu, an affiliate with Fralin Life Sciences Institute’s Center for Emerging, Zoonotic, Arthropod-borne Pathogens.  

This coexistence makes establishing the high phage-to-bacteria ratio needed to treat intestinal infections hard to achieve. 

“That’s extremely challenging to achieve in your gut,” Hsu said. “And then once you have a bacterial infection in your gut, a lot of times it’s just not even accessible to phages. It’s already hidden away in the mucosa or cells of your body; it’s not just free-flowing to where the phages would be able to access them.”  

To work around these impediments, the team engineered a nonpathogenic E. coli bacterium to carry a phage that only infects salmonella. This ensures that when the phage is produced, it can specifically target the pathogen.   

Usually, this type of salmonella phage remains dormant in the salmonella bacterial genome, but Hsu’s team made several genetic modifications so that it is carried by E. coli, and, once it is released into the gut, it automatically kills salmonella in a process called lysis. This process rapidly increases the number of phages to fight the bacteria. The researchers coined this new type of phage-bacterial combination a “lytic phage-producing lysogen,” or “lyto-lysogen.”

Salmonella can typically detect phage DNA produced by non-salmonella bacteria and prevent it from replicating. But in this case, the researchers were able to disguise the phage.

“We were able to trick the salmonella bacteria into thinking the phage from E. coli was ‘not foreign’ by adding a salmonella gene into the E. coli genome,” Bataglioli said. “A phage that comes from our E. coli can infect salmonella, can propagate easily in salmonella, lyse it, and then all the phages that are produced from salmonella can just keep replicating.” 

This rapid reproduction eventually leads to the eradication of the infection from the gut. 

“What happens is that this good bacteria, the E. coli, produces all this antipathogen phage, and there is now a protective lining so that when salmonella comes in, just after passing through the stomach and at its weakest point, it meets this high, killer density of phages,” Hsu said.  

The researchers say they targeted salmonella due to its high global disease burden, as it can kill the elderly, children, and those with HIV; it has a high prevalence of antibiotic resistance; and it has been upgraded to a high-priority pathogen by the Centers for Disease Control and Prevention. They believe this work, however, has strong implications for other illnesses. 

“We’re starting off with salmonella, but expanding, obviously, with the correct adaptations to target other diseases; other bacterial pathogens, would be an interesting route to explore,” Bataglioli said. 

“We have a framework in place that shows that we could potentially put other phages in there and target other bacteria,” Hsu said. 

Bataglioli plans to continue his bacteriophage research with the School of Chemical Engineering at the State University of Campinas in São Paulo, Brazil, in the fall.

Funding for this research was provided by the National Institute of General Medical Sciences of the National Institutes of Health. Bataglioli’s funding was supported by the Postdoctoral Fellowship in Drug Delivery from the PhRMA Foundation. 

Other researchers involved in this study include the following: 

• Hiba Baaziz, Ph.D., lab manager, biological sciences 

• Hallie Avalos, currently a graduate student at Vanderbilt University Medical Center 

• Lindsay Smith, undergraduate researcher, College of Science 

• Zach Baker, Ph.D., current postdoctoral researcher at Colgate-Palmolive 

• Rita Makhlouf, graduate student, biological sciences

• David Da Silva Barreira, Ph.D., current postdoctoral researcher at the University of Wisconsin, Madison 

• Harsimran Kaur, Ph.D., presidential postdoctoral associate in biological sciences 

• Teresa Southard, associate professor at the Virginia-Maryland College of Veterinary Medicine

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Journal

Nature Microbiology

DOI

10.1038/s41564-026-02484-3

Article Publication Date

16-Sep-2026