ERC Starting Grant for Tom Beneke: Drug resistance in tropical parasites

University of Würzburg

Facebook

XLinkedInWeChatBlueskyMessageWhatsAppEmail

 

image: 

Dr Tom Beneke in his lab. The Würzburg researcher has been awarded a grant worth 1,5 millions from the European Research Council for his work on the tropical parasite leishmania.

view more 

Credit: Robert Emmerich / University of Würzburg

Through its Starting Grants, the European Research Council (ERC) supports talented early-career researchers who can demonstrate an outstanding track record and an excellent new research idea.

This is precisely the case for molecular biologist Dr Tom Beneke (35) from the Biozentrum at the University of Würzburg. The ERC has awarded him one of its €1.5 million grants to further advance his research on Leishmania and the disease they cause.

This is yet another great success for the scientist. Just a few weeks ago, the German Research Foundation (DFG) awarded him 2.2 million euros to set up a junior research group. This project also focuses on Leishmania parasites.

“The ERC Starting Grant is a fantastic recognition of our work to date. Together with the recently awarded Emmy Noether grant and other externally funded projects, we can now establish a long-term research programme in Würzburg and investigate key questions about Leishmania biology and the causes of treatment failure in leishmaniasis,” says Tom Beneke.

Drug resistance is on the rise

Leishmania parasites are also found around the Mediterranean. They are transmitted to humans, as well as to dogs and other animals, through the bites of sand flies. Some Leishmania species cause skin ulcers, whilst others mainly affect the liver and spleen – the latter is almost always fatal if left untreated. Every year, up to one million people worldwide develop leishmaniasis, and several thousand die from the disease.

There are no approved vaccines for humans, and the available treatments often cause severe side effects. At the same time, resistance to the few available drugs is increasing.

Parasites can enter a dormant state

In his ERC project ‘PERSIST’, Tom Beneke is investigating the parasites’ drug resistance. Some evade treatment by entering a kind of dormant state inside their host cells. Researchers refer to this as persistence. In this state, the pathogens grow only very slowly or not at all – which makes them even more difficult to target with drugs. As soon as treatment ends or the effect of the drugs wears off, the Leishmania parasites can become active again.

For a long time, researchers regarded this dormant state as a temporary reaction by the parasites to stress caused by the drugs. “However, recent research findings, including those from my group, suggest that certain genetic variations increase the likelihood of the parasites entering a state of persistence,” says Tom Beneke.

Unravelling the genetics of the pathogens

The Würzburg-based researcher aims to identify which Leishmania genes control the switch between active and dormant states in the parasite. He also wishes to clarify whether Leishmania possess a kind of biological memory that makes them particularly prone to repeatedly entering a dormant state. In addition, research will focus on how these mechanisms differ from classic resistance mutations and which genetic changes make Leishmania more susceptible to drugs.

The findings could help to significantly improve the treatment of leishmaniasis. The long-term aim is to develop new combination therapies that not only combat resistance but also prevent the formation of surviving dormant stages, thereby reducing relapses following treatment.

Tom Beneke’s career

Tom Beneke, born in 1990, is from Berlin and studied biotechnology at the Brandenburg University of Technology Cottbus-Senftenberg. After completing his bachelor’s degree, he moved directly to the University of Oxford as part of a fast-track PhD programme without first completing a master’s degree. There, he completed his PhD between 2015 and 2019, focusing on the swimming behaviour of Leishmania parasites.

Beneke then continued his research in Oxford for a short period of time before subsequently moving to the biotech company Oxford Genetics as a specialist in CRISPR screening. However, after just under two years in industry, he decided to return to academic research. In 2022, he joined the Biocentre at the University of Würzburg on fellowships from the European Molecular Biology Organisation (EMBO) and the European Union (Marie Curie). Here, he continued his research on Leishmania.

In 2024, he established an independent junior research group. In addition to the Emmy Noether Programme, this group is funded by further third-party projects. These include another DFG grant, a Horizon Europe project and a grant from the Humboldt Foundation.

A University of Stirling study could pave the way for the more efficient study of the secretions that salmon lice use to avoid fish defences, potentially enabling the development of new strategies to protect salmon from infestations. Research led by PhD

Salmon lice feed on the skin, mucus, and blood of fish, causing open wounds that can lead to infection – reducing the market value of farmed fish and increasing the chance of secondary infections

University of Stirling

Facebook

XLinkedInWeChatBlueskyMessageWhatsAppEmail

 

image: 

Alexander Dindial of the University of Stirling.

view more 

Credit: University of Stirling

A University of Stirling study could pave the way for the more efficient study of the secretions that salmon lice use to avoid fish defences, potentially enabling the development of new strategies to protect salmon from infestations.

Research led by PhD researcher Alexander Dindial alongside Professor James Bron and Dr Sean Monaghan at the University’s world-renowned Institute of Aquaculture, in collaboration with Moredun Research Institute’s Kevin McLean, has resulted in the development of a new and precise way to collect and study secretory and excretory products (SEPs) from salmon lice. This includes substances released from the glands of the lice that make it easier for them to feed or evade their host’s immune system.

Salmon lice feed on the skin, mucus, and blood of fish, causing open wounds that can lead to infection – reducing the market value of farmed fish and increasing the chance of secondary infections.

Various treatments have been developed to tackle sea lice infestations in Atlantic salmon aquaculture – which costs the industry more than $1b a year – but some of these can be expensive, unreliable, environmentally damaging, and negatively impact animal welfare.

Previous methods for extracting SEPs from salmon lice involved pooling together large numbers of individuals, hiding the natural differences between individual lice, which can provide a vital insight for developing targeted treatments or vaccines.

The new method, as well as allowing study of individuals, also reduces the potential for louse faecal contamination. It allows collection of high-quality samples from a single louse per test, with substantial yields of secretory proteins per louse.

Mr Dindial explained: “Salmon lice cause hundreds of millions of pounds of damage annually to the global salmon aquaculture industry through mortality, lost production and the implementation of control measures. Understanding these secretions is an important step towards understanding louse biology and developing new, safe, and effective strategies for control.”

Research involved collecting secretions from individual salmon lice by placing a small drop of solution over their mouths and letting them release proteins into it. These proteins were then examined using a technique called liquid chromatography tandem mass spectrometry to analyse the exact protein composition of each of the samples. This technique uses state-of-the-art equipment to separate the components of a sample, breaking it into fragments and analysing them - revealing protein composition and helping to identify them.

The team found 148 total secretory proteins, 64 of which were detected in each of the tested conditions – some of which could represent potential targets for vaccine development.

The secretory protein profiles of individual lice showed a wide variation in protein number and diversity, a pattern consistent with other ectoparasites like ticks and mosquitoes.

Mr Dindial continued: “This work has the potential to expand our knowledge of salmon louse biology and to provide insight into louse proteins that could be exploited to help fish mount an immune response against infection.

“The novel methodology developed here has the potential to directly facilitate further research into salmon louse secretory biology. It allows for the reproducible, reliable, and efficient extraction of high concentrations of salmon louse secretions, all while minimising faecal contamination.

“As well as improving the study of these secretions, the protocol could be used to investigate how drug or therapeutic treatments might alter louse secretory activity, ultimately advancing efforts to control this parasite.”

The work builds on a first-of-its-kind study led by Mr Dindial, published last year, that uncovered major differences in the secretions that the parasite uses to feed and evade the immune system at different stages of its life cycle.

Investigation of a novel assay for the proteomic screening of the secretory and excretory products of individual salmon lice Lepeophtheirus salmonis was published in Veterinary Parasitology.

This work was funded by EastBio as part of the study lead’s PhD studentship, with a funding contribution from Moredun Research Institute.

Collaborative research was conducted with the project Towards lice-resistant salmon: functional genetics and genome editing to enhance disease resistance in aquaculture, funded by UK Biotechnology and Biological Sciences Research Council (BBSRC), Sustainable Aquaculture Innovation Centre and Benchmark Genetics Limited and involved partners from Roslin Institute at the University of Edinburgh, the Centre for Environment Fisheries and Aquaculture Science. the Atlantic Veterinary College at the University of Prince Edward Island, and Kames Fish Farming Ltd.

---

Journal

Veterinary Parasitology

DOI

10.1016/j.vetpar.2026.110752 

Method of Research

Experimental study

Subject of Research

Animals

Article Title

Investigation of a novel assay for the proteomic screening of the secretory and excretory products of individual salmon lice Lepeophtheirus salmonis

 

Cattle research may provide answers to father’s role in pregnancy loss

Texas A&M AgriLife researcher investigates paternal epigenetics to uncover causes of early pregnancy loss

 - by Kay Ledbetter

When a pregnancy ends early and unexplained, the search for answers usually begins with the mother. Lacey Luense, Ph.D., wants to know what the father’s sperm might have to do with it.

Lacey Luense, Ph.D., an assistant professor in the Texas A&M Department of Animal Science, is studying the male role in early pregnancy loss. (Courtney Sacco/Texas A&M AgriLife)

Luense, an assistant professor in the Texas A&M College of Agriculture and Life Sciences Department of Animal Science, studies the causes of early pregnancy loss — a problem that cuts across species and carries both personal and economic costs.

She is working with cattle, where almost 50% of pregnancies are estimated to end prematurely, to study the root causes of human infertility, where over 50% of all conceptions are estimated not to result in birth.

“We know that maternal issues can be involved,” Luense said. “Sometimes it can be a chromosomal abnormality, disease or problems with the uterine environment. But we don’t know the causes of many pregnancy losses. It’s unexplained, and we are still trying to figure out why this happens so frequently.”

Luense, who also has an appointment with Texas A&M AgriLife Research, is joining forces with Ky Pohler, Ph.D., administrator for the Texas A&M AgriLife Animal Reproductive Biotechnology Center and associate professor, Department of Animal Science, on a $1.65 million National Institutes of Health grant to look at how paternal epigenetic contributions, or non-genetic changes to DNA, are delivered to the embryo.

Determining the male factor in unsuccessful pregnancies

Luense said one potential cause for pregnancy loss could be the male’s sperm and epigenetics — or everything above and around the DNA sequence — that affect how the DNA is structured or packaged.

“We are talking about nongenetic changes that can alter how those genes are turned on or off,” she said. “Our research is trying to understand how dad’s epigenetics or the epigenetic changes carried by the sperm can affect fertility, pregnancy and then long-term health and development.”

The overall goal is to understand the nongenetic changes to DNA that are delivered to cattle embryos. The team will use sperm from bulls of high and low fertility to investigate the role of the paternal epigenome in abnormal embryo development and pregnancy loss.

 

Texas A&M AgriLife research is trying to understand how the male epigenetics can affect fertility and pregnancy. (Laura McKenzie/Texas A&M AgriLife)

One focus is histones, the proteins that DNA wraps around like a spool and thread. Previous studies indicate males with abnormal sperm histones are more likely to have partners who experience pregnancy loss.

“However, we don’t know why that happens,” Luense said. “This is something we have been learning much about over the last decade or two. We know a clinical correlation exists, but we do not understand the reasons it occurs. Determining that is our challenge.”

Cattle can answer questions humans cannot

Luense is determined to help with human pregnancy loss, but experimenting with human embryos is not an option. And, while she has also worked with mouse models, cattle offer something they couldn’t: early embryonic development that more closely mirrors human embryo development, particularly in cell division and timing when genes from the new embryo activate.

Where discovery meets industry

Department of Animal Science faculty are asking questions with answers that reach far beyond agriculture — into human health and everyday life.

Explore the research

Her team will conduct different molecular and genomic analyses on the semen samples from the high- and low-performing bulls to try to understand their biomarkers and to identify changes in the sperm to predict pregnancy loss. 

Through in vitro fertilization, IVF, they will be able to generate embryos from bulls with specific changes to the sperm epigenome. These embryos will undergo time-lapse imaging and cutting-edge genomic analyses to determine if changes to sperm histones alter development and gene regulation. Performing such experiments in humans is not possible, making the use of cattle an exciting opportunity to further our understanding of human fertility and pregnancy, Luense said.

The new Animal Reproductive Biotechnology Center, which opened in 2025, will allow them to perform gene editing, including CRISPR/CAS 9, to advance knowledge about pregnancy loss and how treatments can be developed to solve the issue.

“We are trying to identify changes in gene expression that are happening very early in pre-implantation embryo development in cattle and how that might give us information about what is happening in humans,” Luense said.

The goal of the research is to find ways to achieve a higher rate of live births and calves on the ground. (Michael Miller/Texas A&M AgriLife)

Biomarkers to predict, and someday prevent, pregnancy loss

Beyond the human health question, the findings could give cattle producers new tools to address a costly problem — roughly half of cattle pregnancies do not result in live births. Better prediction could mean real savings for the industry.

“We hope that, after five years, we will be able to identify biomarkers or alterations to sperm chromatin or sperm histones that may predict pregnancy loss in humans and cattle,” Luense said. “If we know what to look for, maybe it can be treated. We are trying to understand the specific gene pathways regulated by sperm epigenetics occurring in the early embryo and are necessary for a healthy pregnancy and a live birth.”

The results could impact reproductive efficiency and help clinical management of human patients and livestock diagnosed with infertility, poor embryogenesis and pregnancy loss, she said.

 

New computational tool finds hidden asthma genes missed by traditional methods

University of Chicago

Facebook

X
Bluesky
Email

One of the most important goals of studying genetics is to find genes that are involved with diseases. The problem is that most diseases aren’t caused by a single gene or mutation. They’re the result of complex interactions among dozens, if not hundreds or thousands of genes, plus environmental factors, lifestyle, and a host of other variables. That flood of genes creates a needle-in-a-haystack problem.

A growing view among geneticists holds that nearly every gene active in the relevant tissue plays some part in a disease, but the vast majority act only indirectly and from a distance, nudging a much smaller set of "central" genes that sit at the heart of the disease. Those central genes are the ones that directly drive the biology and therefore are the ones most worth targeting with drugs. Until now, though, scientists had no reliable way to pick them out of the crowd and experimentally test them.

An interdisciplinary team of researchers at UChicago and Columbia University developed a new computational tool that could make the challenge of finding genes most directly related to disease much easier. In a paper published in Cell, they showed how this tool was able to identify 21 genes related to asthma, most of which hadn’t been discovered by other methods. The researchers also used both CRISPR gene-editing screens and mouse models to validate that these genes lead to asthma phenotypes and demonstrated that two of the genes are in the same pathway involved in fatty acid metabolism and protein palmitoylation, which hasn’t yet been studied for asthma. 

A flowering network of genetic effects

The new tool, called DANDELION, focuses on a process known as trans-gene regulation. In complex diseases like asthma, many genetic variants may contribute to disease by changing the expression of other genes. This has a cascading effect where one variant changes the expression of a nearby gene, and then that gene changes the expression of another, and so on. This creates what’s called a gene regulatory network that ultimately drives the development of disease.

Existing approaches like genome-wide association studies (GWAS) instead focus on genes that are often in the periphery of the gene regulatory network, however, and only indirectly affect disease. 

“All these existing tools assume that the actual disease genes are always going to be very close to the disease variants, but when you search for clues around that variant, you don’t always find much,” said co-senior author Xuanyao Liu, PhD, Assistant Professor of Medicine and Human Genetics, who developed DANDELION.

“What's unique about our method is that we believe the disease genes are not just next to the genetic variants. They're embedded in this gene regulatory network, and the actual disease-driving gene is downstream of those associated variants, maybe on different chromosomes. So, they're on the receiving end of a genetic effect that is very far away,” Liu said.

Liu named the tool DANDELION in reference to the puffy heads of dandelion flowers once they go to seed. The puffball resembles an interconnected, branching network of genes, ultimately pointing to the center of the core disease genes (called disease-proximal genes, or DPGs).

Liu analyzed a large set of data from the human transcriptome and the UK Biobank, a repository of health and genetic data from more than 500,000 volunteers. She used DANDELION to search for DPGs for asthma and found 21 candidates, 19 of which have not been discovered before using tools like GWAS. She showed the data to Marcelo Nóbrega, MD, PhD, Chair of the Department of Human Genetics at UChicago, who has developed experimental platforms to manipulate the expression of genes in human cell types that are relevant to asthma, such as epithelial cells from the lining of the airways, inflammatory cells, and immune T cells.

At first, he was skeptical. “Xuanyao showed me a list of genes, and we didn't recognize almost any of them. I thought that either this is going to be really cool and groundbreaking or it's going to be wrong. But we had the experimental validation system running, so I thought, ‘Let's test them all,’” he said.

Direct, measurable impacts

Nóbrega’s team, led by postdoctoral scholar Isabella Salamone, PhD, conducted a series of experiments to test the effects of the genes predicted by DANDELION. Surprisingly, most of the genes Liu identified had a direct, measurable impact on the function of asthma-related cell types, producing phenotypes that model those seen in asthma at a much higher rate than the distal genes, or any other genes in the genome that they also tested.

When Salamone looked more closely, she saw that two genes had opposite effects. Knocking out one gene called SLC27A3 protected against the effects of asthma in both epithelial and T cells, while knocking out another gene, SCD, contributed to disease. Looking at the effects of mutations of these genes in a large human cohort of almost half a million people, they found that mutations in SLC27A3 are protective of asthma, supporting their findings in their cellular phenotyping screens.

“We saw this really striking pattern. Knocking out SLC27A3 had the strongest protective effect of all the genes we tested, and knocking out SCD was very detrimental to whatever cellular function we assayed,” Salamone said. “When we dug into patient data that had been collected by other labs, we saw the same pattern repeat itself—expression of SLC27A3 is increased in lung cells of patients with severe asthma, and SCD expression is decreased.” 

Intriguingly, both SLC27A3 and SCD are involved in the same biochemical pathway for fatty acid metabolism. To understand how this might be linked to asthma, they turned to chemical biologist Hening Lin, PhD, the James and Karen Frank Family Professor of Medicine and Professor of Chemistry at UChicago, who is a world-leading expert on the process, especially its role in protein palmitoylation, the addition of a long-chain fatty acyl group to proteins that regulate protein activity. Lin helped them confirm that both genes are involved in palmitoylation, and that reducing palmitoylation by knocking out SLC27A3 causes lung epithelial cells to dampen several immune-related and inflammatory processes.

“My lab has been working on the role of protein palmitoylation in immune signaling. We know many immune signaling pathways are regulated by palmitoylation, but I am still amazed by the finding that disrupting a lipid metabolic protein, SLC27A3, could offer protection in asthma models at least in part via affecting protein palmitoylation,” Lin said.

Finally, to test whether these genetic, biochemical, and cellular findings ultimately translate into asthma susceptibility, Salamone developed mice in which SLC27A3 or SCD were inactivated. They found that SLC27A3 knock-out mice are protected against allergy-induced lung inflammation, while SCD knock-out mice are more prone to lung inflammation compared to control mice, demonstrating that the new pathway the team uncovered is indeed capable of changing susceptibility to asthma.

A powerful, interdisciplinary collaboration

Liu said she is encouraged by this initial success and looks forward to testing it with other diseases like inflammatory bowel disease or Type 2 diabetes. Historically, one of the limitations of drug development has been finding the true protein targets for treatment. DANDELION has the potential to overcome this challenge by identifying new and more effective drug targets.

“We're really excited about this direction because for these diseases, GWAS has identified tons of signal, but we still don't know the actual disease-driving genes that we can target for therapies,” Liu said. “I think our collaboration has been really powerful because we closed the gap at both the computational level and the experimental level.”

Nóbrega emphasized the importance of this collaboration as well, especially the advantage of being able to confirm their findings with a leading expert like Lin. “None of this would have come to fruition if any one of us were working on this alone,” he said. “We would have three papers buried in separate journals and virtually nobody would know how to put these stories back together. So, the power of having this complementary expertise across the division is really important.” 

The study, “Trans-regulatory gene mapping prioritizes disease drivers in asthma,” was primarily supported by the National Institutes of Health. Additional authors include Peixin Tian from the First Affiliated Hospital of Kunming Medical University, China; Zining Qi, Jiaqi Zhao, Li Zhang, Qilong Tan, Jinghui Li, Alexis G. Thornburg, Noboru J. Sakabe, Mark Minogue, Zachary T. Weber, Bohao Chen, Cezary Ciszewski, Xin He, Hardik Shah, and Carole Ober from UChicago; Ashley N. Michael and Donata Vercelli from the University of Arizona; and co-senior author Zhonghua Liu from Columbia University.

---

Journal

Cell

DOI

10.1016/j.cell.2026.07.034 

Article Title

Trans-regulatory gene mapping prioritizes disease drivers in asthma

Article Publication Date

20-Aug-2026

 

A viral 'loose cannon' enzyme helps phages shut down bacterial defenses

Scientists have found how phages, viruses that infect bacteria, orchestrate an explosion of protein modifications inside host cells that helps them evade the bacteria’s immune systems

European Molecular Biology Laboratory

Facebook

XLinkedInWeChatBlueskyMessageWhatsAppEmail

 

image: 

Illustration depicting how T7 kinase, a phage enzyme, modifies many proteins inside an infected bacterium, helping shut down its defence mechanisms.

view more 

Credit: Daniela Velasco/EMBL

Scientists have discovered a previously unknown strategy that phages – viruses that infect bacteria – use to disable bacterial defence systems. The strategy relies on T7 kinase, a phage enzyme that sets off an explosion of protein modifications inside infected bacteria, shutting down their defence systems.

Like all viruses, phages exist in a perpetual molecular arms race with their hosts. Bacteria evolve mechanisms to defend against infecting phages, while phages evolve anti-defence systems to shut down or evade these immune mechanisms. The new study demonstrates, for the first time, how a single phage protein can set off a wave of molecular events that can disarm multiple bacterial defences. 

These findings resulted from a long-standing collaboration between two research groups at EMBL Heidelberg – the Typas Group, which specialises in high-throughput studies of bacterial interactions, and the Savitski Team, who are experts in cutting-edge proteomics technologies. 

“Phage research has led to a lot of exciting developments, the CRISPR-Cas9 gene editing system among them,” said Mikhail Savitski, Senior Scientist and Head of Proteomics Core Facility at EMBL Heidelberg. “Using the sensitive technologies we had available in the lab, we wanted to understand in an unbiased way how phages affect bacterial proteins during infection.”

A loose cannon inside the cell

For this, the researchers used a well-known model system – E. coli, a rod-shaped bacterium that lives in our guts, and T7 phage, a virus that infects E. coli. The team decided to look closely at protein phosphorylation in phage-infected bacteria. Phosphorylation is a kind of rapid chemical modification of proteins which can change their function, e.g. by activating or inactivating them. 

Surprisingly, the scientists found that phage infection resulted in almost every single bacterial protein getting phosphorylated within minutes, at least for a fraction of their population within the cell. The likely culprit was T7 kinase, a phage enzyme first discovered in the 1970s. However, the scale of phosphorylation was unlike anything previously observed. In fact, the list of phosphorylation targets for the T7 kinase surpassed what’s known so far for any kinase in nature, leading the researchers to dub it a ‘loose cannon’. 

“We realised that we were seeing a quite unprecedented molecular event: a catastrophic phosphorylation across the entire proteome in a completely nonspecific manner,” said Savitski. “That had never been seen before, and it was fascinating that there was also no pattern to it.”

Shutting down bacterial defences

However, this discovery posed a new question. Previous studies had shown that deleting T7 kinase from the phage’s DNA doesn’t really affect the infection process. “As puzzles go, it leaves you a bit flabbergasted,” said Savitski. “You have a kinase with apparently no phenotype that seems to phosphorylate everything in the proteome.”

The researchers confirmed that the activity of the T7 kinase was short-lived – as previously reported, it inactivates itself within 5-6 minutes post infection. Examining the structure of T7 kinase yielded another important clue: one section of the kinase, called the shutoff domain, was not needed for its phosphorylation activity but was rich in chemical features that might help it bind DNA. This led the team to hypothesise that this domain might help the kinase attach to DNA and subsequently come close to other DNA-binding proteins.

“Methodologically, it is not easy to test such things, but we designed an elegant experiment that could measure exactly how much of a protein population is phosphorylated inside a cell,” said Tara Bartolec, postdoc at EMBL Heidelberg and one of the first authors of the paper. Using this, the researchers found that the T7 kinase preferentially targeted DNA-binding bacterial proteins, phosphorylating and presumably inactivating them.

DNA-binding proteins are often the bedrock of bacterial defence systems, helping them detect and destroy phage DNA inside the cell. And indeed, the researchers found that the kinase could help the virus infect strains of bacteria that had such defence systems. 

By also comparing kinases across different types of phages, the researchers believe they may have hit upon an evolutionarily conserved mechanism that certain phages use to deactivate bacterial immune systems.

In the future, the researchers plan to look at other protein modifications and the role they might play in phage infections. The study also opens up the possibility of novel bioengineering approaches that use these new insights into phage biology to design or predict the effectiveness of phage therapies.

”To be effective for therapy, phages should be capable of infecting diverse versions (strains) of the same pathogen,” said Typas. “Interestingly, pathogenic strains are exquisitely diverse in their immune repertoire, and can always pick up new systems. So engineering phages with broad anti-defence systems, such as the T7 kinase, might be key in this quest for effective phage therapies. We identified the first one here, but we are sure there are many more out there.”

---

Journal

Nature

DOI

10.1038/s41586-026-10934-5 

Article Title

Pervasive phosphorylation by phage T7 kinase disarms bacterial defenses

Article Publication Date

19-Aug-2026