A balanced diet limiting specific nutrients is a tool that helps slow down the ageing processes, maintain good health, and prolong life. Accordingly, in the coming decade, researchers will focus on studying how specific dietary components – such as amino acids, carbohydrates, fats, and microbiota – affect our health and longevity.

Scientists will explore which food components contribute to chronic diseases or even cancer, and how these effects are linked to dietary restrictions, physical activity, and other healthy lifestyle elements. The long-term benefits of limiting specific individual nutrients have already been confirmed. Such diets may offer anti-cancer benefits, slow ageing, protect the cardiovascular system, and improve gut microbiota and brain health.

Health gains associated with methionine

Recently, protein consumption has garnered significant attention in online discussions, which may give the impression that it is the most crucial nutrient for the human body. However, this approach is misleading. To function properly, our bodies need proteins, carbohydrates, fats, vitamins, fibre, and water. To stay healthy and live longer, a proper balance of all these nutrients is essential, along with avoiding over- and under-eating.

Did you know that one of the most essential nutrients for our body is methionine, an amino acid found in proteins? It is vital for the proper development of the body. Simply put, methionine plays a key role in the body’s ability to produce proteins and maintain good health. It also helps combat inflammation and supports healthy tissue function. 

Due to its importance for our metabolism and bodily functions, methionine is essential to the human diet. However, excessive intake of this amino acid through food can lead to many health issues, including atherosclerosis, short-term memory loss, neurodegenerative diseases, and reduced skeletal muscle growth. Therefore, it is advisable to consume methionine in moderation.

A methionine-restricted diet can prolong life

The discovery that long-term methionine limits can increase the lifespan of rats by up to 30% sparked extensive research into methionine-restricted diets. These studies have shown that reducing methionine intake also extends lifespan in other model organisms, such as Caenorhabditis elegans, fruit flies, and mice. This effect is associated with reduced production of reactive oxygen forms, higher levels of cellular antioxidants, and decreased oxidative damage to proteins, fats, and DNA.

Recently, more and more attention has been paid to methionine-restricted diets. This dietary approach can provide a range of benefits: it may offer anti-cancer effects, improve metabolism, slow ageing, stop inflammation, prevent diabetes, enhance insulin sensitivity, protect the cardiovascular system, and support gut microbiota and brain health. 

Methionine is found in plant, animal, and microbial foods, but its concentration varies significantly across different food groups. The highest levels are found in meat, seafood, Brazil nuts, and eggs; moderate amounts are present in dairy products, while fruits and vegetables contain the lowest levels. The ketogenic, Japanese, and vegan diets tend to have the lowest methionine content. Given the wide variation in methionine levels across foods and different diets, there is a growing interest in developing a method for calculating and monitoring dietary methionine intake more precisely.

While methionine restriction offers considerable potential health benefits, it is still crucial to ensure an adequate intake of this amino acid, as too little of it can lead to growth disorders. Therefore, it is essential that the restriction of any nutritional element does not result in an overall deficient diet.

Methionine is a direct target for cancer treatment

An enzyme called methionine adenosyltransferase (MAT2A) produces an important molecule from methionine, known as S-Adenosyl methionine (SAM). This molecule is involved in the DNA modification process called DNA methylation. In basic terms, methylation occurs when a small part of this molecule – a methyl group – binds to DNA. If the body lacks methionine, SAM is not produced, so methylation cannot take place. 

DNA methylation is an essential process that occurs in every human cell. It alters the structure of DNA, which often leads to specific genes being ‘switched off’, meaning they become inactive. This regulates essential processes in the human body, for instance, by ensuring the stability of genetic information. Methylation helps cells perform their unique functions in the tissue during development (e.g. allowing an embryonic stem cell to become a skin, liver, or nerve cell).
This process starts changing as we age: many genes lose their methylation marks, while others become heavily methylated. As a result, some genes critical to cellular function may stop working.

This mechanism of DNA regulation is also important in the case of diseases, particularly cancer. In cancer cells, some genes undergo extensive modifications that impair their function (even when that function is crucial), while others become active when they should not be. This imbalance in gene activity promotes the transformation of healthy cells into cancerous ones. For this reason, methionine – from which the SAM molecule is synthesised – is of significant interest in cancer research.

In fact, nearly 50 years ago, scientists discovered that cancer cells require more methionine from external sources compared to healthy cells. The more aggressive the cancer cells are, the more dependent they are on this amino acid to sustain their activity. Therefore, limiting it in food can be one of the new avenues for cancer treatment.

The levels of methionine in the body can be reduced in two ways: by following a special low-methionine diet or by using a protein called methioninase as a drug to break down methionine. Studies show that lowering methionine levels and simultaneously applying chemotherapy or radiotherapy can lead to better treatment outcomes.

Clinical trials are underway to investigate how limiting this amino acid affects cancer cells and their environment: immune cells, blood vessels, and connective tissue cells. However, many details still need to be clarified.

Vilnius University researchers develop a method for detecting epigenetic changes

Three key proteins operate in our bodies – DNA methyltransferases, also known as epigenetic ‘writers’ because they can ‘write’ the epigenetic code by modifying DNA, thereby altering the functioning of the cell. These enzymes are called DNMT1, DNMT3A, and DNMT3B. Two of them – DNMT3A and DNMT3B – create new ‘marks’ that determine a cell’s function, while DNMT1 ensures that these ‘marks’ are preserved and passed on to daughter cells during cell division. This process is crucial for normal development and health.

However, when the activity of these methyltransferases is disrupted, the consequences can be severe, triggering, for example, cancerous processes. In such cases, genes that should suppress tumours are ‘switched off’, while cancer-promoting genes become overly active. As a result, cells ‘forget’ their original function and turn malignant. These types of changes are found in many forms of cancer, including those affecting the blood, lungs, liver, and colon.

Until now, it has been challenging to study how each DNA methyltransferase works, but scientists at Vilnius University’s Life Sciences Center and the Faculty of Chemistry and Geosciences have developed a new method that allows researchers to precisely identify how each of these ‘writers’ affects DNA.

A breakthrough in research 

Scientists have developed modified molecules capable of ‘tagging’ DNA in a way that reveals the activity of a specific enzyme. To deliver these molecules into cells, they used electroporation, a technique which temporarily opens up pores in the cell membrane using an electric field. These pores allow the modified molecules to enter the cell and ‘record’ information about DNA modifications.

Developed by researchers from Vilnius University, this method is the first in the world to easily and accurately distinguish the activity of the three methyltransferases under minimally invasive conditions and determine the specific effects of the DNMT1 enzyme. In addition, the scientists devised a less invasive approach by using chemically modified methionine analogues, i.e. molecules that easily pass through the cell membrane and are converted inside the cell into a modified SAM molecule. This enables the regulation of DNA modifications by altering the concentration of methionine in the cell environment. As a result, this method can be applied to detect epigenetic differences in cancer cells under methionine-restricted conditions.

It allows researchers to precisely monitor each methyltransferase's activity and better understand how epigenetic changes contribute to cancer development. Moreover, this technology can be used to study DNA changes in individual cells, tissues, and even throughout the body. It can be applied to various cancer models and used to study DNA, RNA, and protein modifications.

The new methodology represents a significant step forward in cancer biology research, offering a deeper understanding of the disease and potentially leading to more effective treatments in the future.

This research was supported by the Research Council of Lithuania (LMTLT), project No. MIP-23-108, “DNMT1-Selective DNA Methylation Mapping in Tumor Cells Using Preclinical Cancer Models”, and the Vilnius University Young Scientists’ Ideas Project, “Application of Cascade MAT2a-DNMT Genome Tagging Strategy in Cancer Cells”.

Dr Constantinos Patinios, a researcher at the EMBL Partnership Institute operating at the Vilnius University Life Sciences Center (VU LSC), has been awarded the prestigious European Molecular Biology Organization (EMBO) Installation Grant. This recognition is given to promising early-career researchers establishing new research groups in European countries and marks an important international acknowledgment of life sciences research conducted in Lithuania.

Dr C. Patinios’s project, “Pause-Repair-Edit: A New Paradigm for Genome Editing”, aims to develop novel approaches for genome editing that could substantially expand the application potential of modern genome editing technologies. The EMBO grant – €50,000 per year for five years – will enable the establishment of an internationally competitive research laboratory in Vilnius and further strengthen Lithuania’s position in the rapidly evolving field of genome editing.

Searching for natural genome editing mechanisms

Although molecular biology has advanced rapidly over recent decades, most microorganisms remain genetically difficult to access. As a result, scientific research has long focused on so-called model organisms – not because they are the most biologically or biotechnologically promising, but because they are the easiest to genetically modify.

The research group led by Dr C. Patinios seeks to fundamentally change this paradigm. His project “Pause-Repair-Edit: A New Paradigm for Genome Editing” is focused on developing universal genome editing tools that could be applied to a much broader range of microorganisms than is currently possible with existing CRISPR-Cas technologies.

“Most CRISPR systems used today, such as Cas9 or Cas12a, induce double-strand DNA breaks, which are lethal for many microorganisms. We are looking for a safer, non-toxic path – one that activates the cell’s natural DNA repair mechanisms without causing cytotoxic stress,” explains the researcher.

A new approach to genome editing

Instead of inducing double-strand DNA damage, the strategy developed in his laboratory is based on halting DNA replication. This is achieved by installing ‘bulky’ chemical modifications on DNA that can physically block DNA replication and thereby trigger the microorganism’s internal DNA repair pathways, particularly homologous recombination.

Importantly, this approach avoids DNA breaks that are fatal to the cell and opens the possibility of editing bacterial genomes that have so far been considered virtually inaccessible to genetic manipulation.

As the genome editing technologies are further developed, Dr C. Patinios’s group is also performing fundamental research to better understand the mechanisms behind DNA replication arrest and restart, and to identify new, previously unknown DNA repair pathways.

The results of this research could have a significant impact on microbiome studies, synthetic biology, and industrial biotechnology – from the development of advanced bioproducts to more sustainable biomanufacturing and new solutions in healthcare.

Membership opening international opportunities for VU LSC researchers

The EMBL Partnership Institute operating at VU LSC is part of the European Molecular Biology Laboratory (EMBL) network, which Lithuania joined in 2019. The institute’s mission is to develop high-level international fundamental and applied research in the fields of genome editing and CRISPR-Cas technologies, while strengthening the international visibility of Lithuanian scientists.

The institute promotes close collaboration with EMBL and other partnership institutes, facilitates researcher and student mobility, the transfer of international expertise, and access to advanced scientific infrastructure at both VU LSC and EMBL. This partnership contributes to the growth of VU LSC’s scientific potential and to the integration of Lithuanian life sciences into the European Research Area.

Although different grant cycles vary, in general, the process of applying for grants takes time. According to 2022 European Research Council (ERC) Starting grant winner Dr Stephen Knox Jones Jr, a biochemist at Vilnius University (VU) Life Sciences Center (LSC), it was six months before the application deadline when he started putting words on paper. However, the intellectual work began much earlier. Apart from timing, the researcher shares what other factors are essential in applying for grants.

Receiving a grant as outside validation

"If you want to make a big impact, you need the money to do it. That means applying for grants, which is not an easy process. It takes time. It takes effort. It takes a lot of planning. Getting this grant affirms that these efforts were worthwhile," – says Dr Jones, last year receiving the ERC Starting grant of 1.2 million Euros.

It is not the first grant of this size that he applied for in his life. Before leaving his home country, the USA, Dr Jones applied for another grant he barely missed: “Many people would have said it was a huge waste of my time. However, everything I learnt in that process, I applied here. So indirectly, not getting the first grant helped me achieve another this time around. That is why I suggest thinking with a ‘long-term’ perspective.”
Dr Stephen Jones earned his PhD degree from Brown University (Providence, RI, USA) and later joined Ilya Finkelstein's lab as a postdoc at the University of Texas (Austin, TX, USA). In 2021 he came to VU LSC’s new EMBL Partnership Institute to establish The Jones Laboratory; his team researches and develops novel genome editing tools. For the leader of the Jones!Lab, this was his last and only opportunity to apply for the ERC Starting grant, which is explicitly directed towards new research team leaders with less than seven years since receiving their PhD.

"When you are still quite a young researcher and new to leading a team, it's helpful to have outside validation. You feel a lot of doubt in general, so having other people say you are doing it right is beneficial. Getting the grant is reassuring and motivating. The idea of funding put a lot of pressure on me, but I can breathe a little now," – says the ERC grantee.

Getting as much criticism as possible

Concerning the application timeline, the most important date is the submission deadline. Yet, there are several steps before the applicant gets a final answer almost a year later.
"I started working on it in the summer of 2021, basically six months before submitting. However, that doesn't mean I hadn't been intellectually working on it before. But this was when I started first putting words on paper," – claims the leader of the Jones!lab.

According to him, if you want to succeed with these things, you best get as much criticism as you can, as early as you can: "After writing the application, you need feedback from your peers. It’s tough if you haven't learned how to handle criticism. However, it is better to receive feedback from your colleagues when you can still make changes, than from the ERC committee when you can’t do a thing about it. So if an expert you trust says that your idea needs work or isn’t good enough, it is good to know – you can prepare another one instead."

He suggests that sharing ideas with other people can get you an outside perspective and assure that you are communicating your ideas effectively, helping you develop your ideas further. Of course, it takes time. That is why Dr Jones planned time to build his concept twice. This is a good strategy, as one gets valuable feedback the first time around, enabling a better product the next time. The main goal is to get that information.

"The minimum you need in this process is two people: yourself and a representative from a European university committed to hosting you. But the more people involved, the better. I had everyone from my institute and other close colleagues viewing my work, even people doing similar work in other parts of the world. And, of course, I lined up a team of experts tangential to my project. I asked if they could provide support if needed. So, a more realistic number would be 10 to 20 people," – tells the researcher.

Convincing different audiences

"After submitting the application in January, I didn't hear anything until the summer. Only then I received the first answer. In my case, they sent a positive letter, but I still had to wait for the interview in the fall."

During the interview in September, Dr S. Jones had to present his project in just ten minutes, before answering his panel’s questions: "Here you have all these questions and comments from experts, and from other reviewers who are not experts in your field. It's worth realizing – this is a very broad audience. So, before the interview, I presented my work to people from all different levels of expertise to get feedback: from the top people in my field, those who are experts in other fields, students that just joined my lab, to people who have never heard of CRISPR".

According to him, if you can explain your project to anyone, you truly know your thing. Finally, only in November did the researcher discover he had succeeded.

Convince yourself and use the previous examples

"The crucial thing during the process is trusting that you can do it. But you can't always get that from yourself, so you need a support structure telling you you’re worth it. It gives you the energy you need because it will be difficult," – assures the researcher.

Since there is also a lot of planning and thinking involved, your support team – family, friends, colleagues – will help you make it through the whole process. Even so, one has to believe in himself (herself) too, because if you haven't convinced yourself, you are going to have a hard time convincing anybody else.

"From a more practical perspective, I would advise: don't reinvent the wheel. Many others have made it through this process, so you need to get information from someone like me who has received the grant, or maybe from another colleague who has reviewed that type of application. The people from the research project division also help by sharing examples of prior ERC grants that have been funded and the information on everything you should know," – says Dr S. Jones.

Last but not least, the applicant has to be ambitious: "You want to make sure that whatever you are proposing has a lot of potential for the community. If it can make a big impact, it opens you up to bring in some risk. People should see that the stuff that I do is worth doing".

In 2022 Dr S. Jones and his team received a €1.2 million grant from the ERC. Spanning the next five years, the researcher will lead a project which aims to improve gene editing techniques.

Prof. Patrick Pausch from the Life Sciences Centre—European Molecular Biology Laboratory (LSC-EMBL) partnership institute at Vilnius University (VU) has been awarded a prestigious European Research Council (ERC) Starting Grant of €1.5 million for his innovative research project "Jumbo Phages in Translational Enzyme Research" (JUPITER). Over the next five years, Prof. Pausch and his team at VU will explore jumbo phages—a class of large viruses that infect bacteria—by studying their uncharacterized genes and potential applications in biotechnology.

Advancing Biotechnology

Jumbo phages are viruses with genomes up to ten times larger than typical phages. Only recently has the diversity of jumbo phages been recognized, and much of the genetic content remains unexplored, considerably limiting the understanding of their biology and potential applications. The JUPITER project aims to bridge this gap by employing a novel high-throughput strategy to annotate the functions of unknown genes within jumbo phages.

"This grant offers a unique opportunity to push the boundaries of what we know about jumbo phages. I believe it could lead to groundbreaking molecular tools and methods that may be biotechnologically valuable," said Prof. Pausch.
Prof. Pausch's research is expected to provide new insights into how jumbo phages modulate genetic material and hijack the gene expression machinery of their bacterial hosts. By understanding these processes, the project aims to inspire new antimicrobials, particularly against drug-resistant bacteria, and to create innovative genome-editing tools with wide-ranging applications—from treating genetic diseases to improving agricultural crops.

"Phages are remarkably skilled at taking control of bacterial cells," explained Prof. Pausch. "By studying underexplored genes, we hope to discover new mechanisms and functions that could lead to exciting applications in biotechnology."

Expanding Phage Diversity for Future Discoveries

The large genomes of jumbo phages contain many genes of unknown functions, potentially holding the key to major scientific advancements. "Jumbo phages are big viruses that attack bacteria, and understanding their genes at a large scale will help us to understand their biology in greater detail," said Prof. Pausch. He also noted that the term "jumbo" comes from the famous giant elephant named Jumbo, a name now used to describe other large things, such as jumbo jets.

A key goal of the JUPITER project is to expand the known diversity of jumbo phages. This could accelerate scientific discovery by revealing a broader range of biological mechanisms. Prof. Pausch's collaborative work will include leading researchers from Vilnius University, Drs. Eugenijus Šimoliūnas and Darius Kazlauskas, and provide opportunities for both graduate and undergraduate students to participate, contributing to the development of future scientific talent.

"Together with my team, we are planning to explore the environments of Lithuania to discover new phages and their host bacteria. I am particularly excited to sample previously overlooked environmental niches across the country."

Lithuania and Vilnius University: A Growing Hub for Life Sciences

Prof. Pausch's selection marks a significant achievement for Lithuania and VU. The ERC Starting Grant is one of Europe's most prestigious research funding opportunities, awarded to early-career researchers. For the 2024 ERC Starting Grants, 3500 applications were submitted, and only 495 were selected for funding after two selection rounds. These grants are awarded to researchers 2-7 years after the award of their Ph.D. degree.

"Receiving an ERC Starting Grant is a unique opportunity since grants that fund 'high-risk, high-gain' research at such a scale are quite rare. To succeed in an ERC project, everything needs to align perfectly: the principal investigator, the team members and their institution. Securing another ERC grant further demonstrates that Vilnius University, its researchers, and Lithuania are at the forefront of European research." concluded Prof. Pausch.

This year, two Vilnius University scholars became ERC grantees. Apart from Prof. P. Pausch, another Starting Grant was awarded to Prof. Mantas Šimėnas, working in the Faculty of Physics. Before then, Lithuania had only received one other ERC research grant for early-career researchers in 2022 by Prof. Stephen Knox Jones from Vilnius University, LSC-EMBL.

Scientists from Vilnius University's (VU) Life Sciences Centre (LSC) have discovered a unique way for cells to silence specific genes without cutting DNA. This groundbreaking research, led by Prof. Patrick Pausch and published in the journal Nature Communications, reveals a new way how to silence genes that is akin to pressing a "pause" button on certain genetic instructions within cells.

The research team, including doctoral student Rimvydė Čepaitė, Dr. Aistė Skorupskaitė, undergraduate Gintarė Žvejyte and Prof. P. Pausch at Vilnius University, working alongside an international team, uncovered how cells use a specific system to locate and silence unwanted DNA. This system, which could eventually enable safer gene modifications, shows promise for repairing faulty genes that cause diseases.

“Unlike the well-known CRISPR gene-editing system, often described as molecular 'scissors,' the newly studied type IV-A CRISPR system does not cut genes. Instead, it uses an RNA-guided ‘effector’ complex to recruit an enzyme called DinG, which moves along DNA and silences targeted genes in a more subtle manner.” explains Prof. P. Pausch.

According to the researcher, it is fascinating how the system recognizes the precise location on the DNA to begin working: “The system uses two proteins (Cas8 and Cas5) to find a very short sequence motif adjacent to the RNA guide's complementary target DNA. Once both proteins recognize this short sequence, they melt the double-stranded DNA for target sequence interrogation.”

A critical component in this process is the formation of R-loops—open DNA structures where RNA binds, signalling the system to initiate gene silencing.

“The ‘R’ in R-loop stands for RNA. All DNA-binding CRISPR-Cas systems use this structure to probe the DNA sequence and identify the correct target site. Stable R-loops only form in the presence of a DNA sequence that sufficiently matches the guide RNA. The R-loop essentially tells the system when it's appropriate to start silencing a gene,” states the research professor.

In his words, the DinG enzyme further enhances gene suppression by unwinding the DNA strands, allowing the system to exert its effect over a longer DNA sequence.

This discovery opens doors to future applications in genome editing without the risk of DNA cuts, which could lead to more precise tools for research and biotechnology. “Our system’s unique ability to traverse DNA without cutting genes is intriguing for advanced gene-editing applications,” adds Prof. P. Pausch, who believes this new approach could benefit society by enabling safer genetic modifications.

This illustration shows the final model of the type IV-A mechanism. From left to right: Step 1 shows the formation of the "effector" complex, consisting of guide RNA and type IV-A proteins (rendered from a cryo-EM structure). The RNA-protein complex binds to a short motif next to the DNA target site (PAM). In Step 2, an R-loop forms, signalling the target site is found. Step 3 shows the binding of DinG (pink bubblegum-like structure). In Step 4, DinG likely moves along the DNA to silence the gene, potentially repeating the process for further silencing (Step 5).

Scientists at Vilnius University’s Life Sciences Centre (VU LSC), together with colleagues from the Weizmann Institute of Science (Israel) and Harvard Medical School (USA), have uncovered a previously unknown type of immune signalling molecule produced by the Thoeris II defence system in bacteria — a major finding published today in Nature. The study, entitled “TIR domains produce histidine-ADPR as an immune signal in bacteria”, was led by Dr Giedrė Tamulaitienė’s research group.

This newly identified molecule is remarkable for its unique structure, linking two biologically essential components: histidine, an amino acid used to build proteins, and an adenine nucleotide, a building block of RNA. Until now, all known signalling molecules were composed solely of nucleotides. This discovery significantly broadens the scientific understanding of the diversity of immune signalling mechanisms in nature.

Like humans, animals, and plants, bacteria are constantly threatened by viruses. Over the course of evolution, they have developed a wide range of defence systems – some of which served as the evolutionary precursors to immune system components in higher organisms. Interest in bacterial antiviral systems surged after their applications were realised in genetic engineering. Landmark examples such as restriction–modification systems and CRISPR-Cas "molecular scissors" have even been recognised with Nobel Prizes.

Scientists have identified over 250 distinct antiviral defence systems in bacteria. Following previous work by Vilnius University researchersshowing that small molecules can serve as infection signals within these systems, attention turned to exploring the diversity of such signalling mechanisms.

Discoveries like this not only deepen understanding of bacterial immune strategies but also lay the groundwork for innovations in genetic engineering, biotechnology, and even the development of new antibacterial therapies.

In this latest study, Dr Tamulaitienė’s group closely examined the Thoeris II system, composed of a sensor protein (TIR), which detects viruses, and a transmembrane effector protein (Macro), which receives the signal and triggers a response. Upon detecting viral infection, the TIR sensor synthesises a unique small molecule signal – His-ADPR.

“This ‘message’ – the signalling molecule – is recognised by the system’s effector, the Macro protein, which is embedded in the bacterial cell membrane,” explains Dr Tamulaitienė. “Once it receives the signal, the Macro proteins start to assemble with each other, damaging the cell membrane. In this way the infected bacterium sacrifices itself before the virus can replicate, allowing neighbouring bacteria to survive and preserve the population.”

Using X-ray crystallography, the VU LSC team determined the structure of the effector protein bound to the new signalling molecule. Meanwhile, the team at the Weizmann Institute confirmed that this molecule is indeed synthesised in bacteria upon viral infection. Researchers at Harvard Medical School revealed the structure of a viral anti-Thoeris ‘sponge’ protein – a countermeasure the virus uses to evade the defence system – with His-ADPR bound inside.

The research published in Nature was carried out by Dr Giedrė Tamulaitienė’s team in collaboration with leading global experts in bacterial antiviral systems – Professor Rotem Sorek (Weizmann Institute of Science, Israel) and Professor Philip Kranzusch (Harvard Medical School, USA). The main body of research at VU LSC was conducted by PhD student Džiugas Sabonis, with valuable contributions from PhD student Deividas Vilutis, Audronė Rukšėnaitė, Dr Arūnas Šilanskas, and Dr Mindaugas Zaremba.

The Weizmann Institute team consisted of Carmel Avraham, Ehud Herbst, Azita Leavitt, Erez Yirmiya, Ilya Osterman, and Gil Amitai. The research at Harvard Medical School was carried out by Renee Chang, Allen Lu and Hunter Toyoda.

Nature is among the most highly cited and prestigious scientific journals in the world. It publishes the best peer-reviewed research across all areas of science and technology, selected for its originality, significance, interdisciplinarity, relevance, accessibility, and often surprising conclusions.