Bacterial blight (BB) is a serious plant disease that mainly affects rice plants, especially in warm, humid regions. Due to the severity of BB, discovering and applying BB-resistance genes is strategically important for ensuring stable rice production in Asia. However, genetic strategies to improve disease resistance face a trade-off between crop yield and immunity to disease—since better immunity may be associated with lower yield.

To date, most BB resistance genes (Xa) that have been “cloned”—i.e., identified, isolated, and functionally validated—either originate from wild rice relatives or are loss-of-function mutations in susceptibility genes, suggesting that BB resistance may have been negatively selected during rice domestication.

Despite this finding, researchers have recognized the importance of elucidating how resistance genes and their regulatory networks are differentially selected during domestication in order to guide disease resistance breeding in rice.

To achieve this goal, Prof. He Zuhua’s team from the Center for Excellence in Molecular Plant Sciences of the Chinese Academy of Sciences, along with Prof. Chen Gongyou’s team from Shanghai Jiao Tong University and Prof. Deng Yiwen’s team from Zhejiang University, have cloned the broad-spectrum BB resistance gene Xa48. They elucidated a new model for broad-spectrum, durable BB resistance involving an NLR immune receptor and its cognate effector, and revealed the molecular mechanism by which XA48 coordinates growth and immunity during crop domestication.

Through large-scale germplasm mining, the researchers identified a novel BB resistance gene, Xa48, in the indica rice variety Shuangkezao (SKZ). Combining map-based cloning with GWAS analysis, they cloned the gene and showed that it encoded an NLR receptor protein. Screening and functional characterization identified its pathogenic cognate effector, XopG, and demonstrated that XA48 directly recognized XopG, thus triggering immune responses.

Systematic genetic, biochemical, and cell biology studies revealed that upon XopG recognition, XA48 promoted degradation of the downstream immune suppressor OsVOZ1/2, ultimately activating immune responses. This discovery provides a foundation for breeding high-yielding, disease-resistant rice varieties.

Moreover, the researchers investigated the domestication trajectory of XA48 to understand how it balances growth and immunity. They discovered that the gene encoding the downstream transcription factor, OsVOZ1, has evolved into two allelic variants: OsVOZ1A and OsVOZ1S. Japonica rice carries only OsVOZ1A, while indica rice has retained both.

The combination of Xa48 and OsVOZ1A imposed a reproductive penalty in japonica—an effect not seen in indica, ultimately leading to the functional loss of Xa48 in japonica. Accordingly, Xa48 was present only in indica (regardless of the OsVOZ1 variant), which is primarily grown in Southeast Asia, a region with high BB incidence. This geographic distribution was consistent with negative selection acting on the resistance gene in japonica, which is traditionally grown in Northeast Asia with lower BB incidence.

Furthermore, the researchers established an immune research platform centered on two major plant immune pathways—pattern-triggered immunity (PTI), mediated by RaxX-XA21, and effector-triggered immunity (ETI), mediated by AvrXa48-XA48—to systematically investigate their synergistic effects during pathogen infection. They developed a comprehensive PTI+ETI platform that integrates these immune networks to improve BB resistance. They also reconstituted broad-spectrum resistance from wild rice into modern rice, offering a novel strategy for sustainable control of crop diseases.

This study lays the foundation for advancing plant protection and crop breeding in China by providing genetic resources and technical support for improving crop disease resistance as part of rice breeding programs.

Investigating a common gene in three very different species—salamanders, mice and zebrafish—scientists have discovered the potential for a novel gene therapy aimed at eventually regrowing limbs in humans, according to new research published this week.

“This significant research brought together three labs, working across three organisms to compare regeneration,” said Wake Forest Assistant Professor of Biology Josh Currie, whose lab studies the Mexican axolotl, a salamander. “It showed us that there are universal, unifying genetic programs that are driving regeneration in very different types of organisms, including salamanders, zebrafish and mice.”

The research, now published in the Proceedings of the National Academy of Sciences, included David A. Brown, a plastic surgeon who studies digit regeneration in mice at Duke University, and Kenneth D. Poss, who studies fin regeneration in zebrafish at the University of Wisconsin–Madison.

Each year, around the world, more than 1 million limb amputations occur because of vascular diseases such as diabetes, traumatic injuries, cancer or infections, according to annual Global Burden of Disease statistics. The number is expected to rise with the aging population and the increase in diabetes diagnoses.

That looming challenge has inspired Brown, Currie and Poss to search for a treatment beyond prosthetics, for something that could replace the complex senses and motor skills of an actual limb.

They might have found the start of a solution in something called SP genes, which the scientists discovered are vital for limb regeneration and shared by the mouse, zebrafish and axolotl.

Therapy makes up for missing gene

The scientists chose to study these three animals for specific reasons:

• The axolotl excels at regeneration, with the ability to regrow complete limbs; tails, including the spinal cord; parts of the heart, brain, liver, lungs and jaw.
• Zebrafish offer one of the best models for appendage regeneration because their tail fins regrow rapidly and have unlimited capacity for regrowth. The zebrafish also can regenerate its heart, spinal cord, brain, retinas, kidneys and pancreas.
• Mice represent mammals like humans, and they already can regenerate the tips of their digits. Humans, too, can regrow their fingertips when an injury preserves the nailbed. That allows regrowth of flesh, skin and bone.

Currie said that once the scientists determined the regenerating epidermis, or skin, of all three species expressed the SP genes SP6 and SP8, they set out to test what the genes do and how they work.

Biology Ph.D. student Tim Curtis Jr. contributed to the research in the Currie lab, with assistance from undergraduate researcher Elena Singer-Freeman, a Goldwater Scholar and 2025 Wake Forest biochemistry and molecular biology graduate.

Emulating the abilities of salamander genes

In salamanders, SP8 does the work in regenerating limbs. Using CRISPR gene-editing technology, Currie’s lab removed SP8 from the axolotl genome. Without SP8, the axolotl could not properly regenerate the limb bones; a similar result occurred with the mouse digits missing SP6 and SP8.

With that information in hand, Brown’s lab used a tissue regeneration enhancer found in zebrafish to develop a viral gene therapy.

That therapy delivered a secreted molecule called FGF8, a gene that is usually turned on by SP8, to encourage digit bone regrowth and partially restore the regenerative effects of the missing SP genes in mice.

Human limbs don’t have that kind of regenerative power—but might someday, with a therapy that emulates the abilities of SP genes.

“We can use this as a kind of proof of principle that we might be able to deliver therapies to substitute for this regenerative style of epidermis in regrowing tissue in humans,” Currie explained.

Building the foundation for human therapies

Although it will require much more research to take the findings from mouse digits to human limbs, Currie called this study foundational in the search for therapies to regrow limbs after injury or disease.

“Scientists are pursuing many solutions for replacing limbs, including bioengineered scaffolds and stem cell therapies,” Currie explained. “The gene-therapy approach in this study is a new avenue that can complement and potentially augment what will surely be a multidisciplinary solution to one day regenerate human limbs.”

He said the decision to collaborate among scientists studying such different animals made all the difference in this research.

“Many times, scientists work in their silos: we’re just working in axolotl, or we’re just working in mice, or just working in fish,” Currie said. “A real standout feature of this research is that we work across all these different organisms. That is really powerful, and it’s something that I hope we’ll see more of in the field.”

Bacterial sensors usually rely on emitting light to transfer information about what they’re sensing, but that method isn’t practical in many settings. That’s why most information transmission is done via electricity. And while electricity-emitting bacteria exist, manipulating them into useful sensors has been quite challenging. Rice University professor Caroline Ajo-Franklin’s group, working in collaboration with researchers from Tufts University and Baylor College of Medicine, recently developed a flexible bioelectrical sensor system called electroactive co-culture sensing system (e-COSENS). The study is published in Nature Biotechnology.

“Bioelectrical sensing is by no means a new concept,” said Ajo-Franklin, the Ralph and Dorothy Looney Professor of Biosciences and corresponding author on this paper. “But e-COSENS is the first system that allows us to easily engineer bioelectronic sensors in a modular manner, like assembling Legos, allowing us to potentially use them to monitor everything from human health to environmental contaminants.”

Bioelectrical sensing requires bacteria that produce electricity and are easy for researchers to manipulate to respond to different substances. Ideally, the bacteria would be able to live in a variety of different places so that the system could be used in environments ranging from rivers to milk.

The challenge was finding bacteria that met all three conditions. E. coli, for example, is simple to engineer but doesn’t produce electricity. L. plantarum, a common food bacterium, produces electricity using a molecule called quinone but is incredibly difficult to engineer.

“Instead of forcing a single bacterium to do everything, we split the job between two bacteria,” said Siliang Li, the first author on this study and postdoctoral fellow. “That division of labor is what makes e-COSENS so flexible and powerful.”

The key to e-COSENS is quinone, the molecule L. plantarum uses to create electricity. L. plantarum cannot create its own quinone; it has to be provided by the environment. This means the quinone can be used as a signal, or trigger, to turn electricity on or off.

The researchers revealed that they could easily manipulate bacteria like E. coli, a bioengineering workhorse, to make quinone only in the presence of a specific substance called an analyte. Once E. coli released the quinone in the environment, L. plantarum would use it to send an electrical signal, which could be read by an electrode—in this case, a current meter.

To test this system, the researchers designed systems to look for four different analytes in four different environments. They used E. coli to sense heavy metal ions in bayou water and inflammation markers in artificial saliva, and L. lactis, another quinone-producing bacterium, to sense antimicrobial peptides in human fecal-derived samples provided by Baylor and an antibiotic in milk from the grocery store. They placed each sample and bacterial system into individual reactors connected to current meters. Within a few hours, all four current meters showed an electrical charge, revealing the bacteria were responding to the analytes—some in as few as 20 minutes.

All four versions of the system were successful, but the large reactors they used wouldn’t easily translate from the lab to the outdoors. Luckily, their collaborators at Tufts had a solution: a compact electronic disk roughly the size of a quarter which can be paired with commercially available digital multimeters.

“This simplified hardware dramatically lowers the barrier to using bioelectronic sensors outside the lab and opens possibilities for low-cost, field-ready diagnostics,” Li said. The researchers had also identified multiple other bacteria that could either send or receive a quinone signal, increasing the number of possible environments e-COSENS could be used in.

“The strength of e-COSENS is the flexibility derived from sharing the work across multiple cells,” said Ajo-Franklin, director of the Rice Synthetic Biology Institute, which focuses on supporting interdisciplinary research. “In the same manner, the success of this research hinged on sharing expertise and work among my research group and our partners, Duolong Zhu and Robert Britton at Baylor and Kundan Saha and Sameer Sonkusale at Tufts.”

Researchers from the University of Seville (US) and the Polytechnic University of Madrid (UPM) have demonstrated that it is possible to grow tomatoes and generate solar energy simultaneously, a key strategy for tackling global water scarcity. The study, carried out in Madrid and Seville during the spring of 2024, evaluated the use of agrovoltaic systems and regulated deficit irrigation to optimize water resources in tomato cultivation. The results show that, although using less water reduces the volume of the harvest, the overall outcome is a more efficient and sustainable process.

This innovative combination aims to reduce the plants’ evaporative demand through the shade provided by photovoltaic panels, enabling a more efficient use of land and water. The research compared three irrigation methods: a control group with full irrigation, a regulated deficit irrigation (RDI) system based on the plant’s water status, and an agrovoltaic (AG) system that applied the same water restriction under solar panels. The study measured variables such as leaf water potential and gas exchange to monitor plant stress at different growth stages. The results indicate that, although the shade from the panels reduces available radiation, the design of the system permits adequate plant development to be maintained at most stages of the crop cycle.

One of the most notable findings is that the deficit irrigation strategy reduced water consumption by approximately 50% compared to traditional irrigation. However, this drastic reduction in water led to a yield decrease of around 20% in the RDI treatment, attributed mainly to severe water stress conditions during the ripening phase. Despite this drop in total tomato production, irrigation water productivity increased significantly in the Seville treatments, demonstrating that more fruit can be obtained for every drop of water invested.

Furthermore, the overall success of the agrovoltaic system was validated by the Land Equivalent Ratio (LER), which combines the efficiency of agricultural and electricity production. The values obtained—1.54 in Madrid and 1.67 in Seville—confirm that combined production is far more efficient than growing tomatoes and generating energy on separate plots. This implies that, although tomato yield decreases under the panels, the system’s profitability and sustainability increase thanks to the generation of clean energy in the same space.

In conclusion, the study highlights that agrovoltaics is a promising tool for the agriculture of the future, although it requires more precise irrigation management to avoid excessive stress. The researchers suggest that combining plant measurements with soil moisture sensors could further optimize these systems. This advance points to the sustainable dual use of land, offering a viable solution to the challenges of climate change and the energy transition.

The results are published in Agricultural Water Management.

While the Netherlands was in lockdown because of the coronavirus, Ph.D. candidate Koen Rijpkema began his research into the same virus. In the lab, he developed molecules that can inhibit an important viral enzyme.

Rijpkema started his Ph.D. in the middle of the pandemic, complete with lockdowns and curfews. “I lived with seven other people, plus visiting partners. At one point, I was in quarantine more often than not,” he says. Working from home was hardly an option, because his research depends heavily on lab experiments.

The coronavirus did, however, offer a highly relevant research topic. “I really wanted to do a lot of synthesis: designing and making new molecules, ideally with the same supervisor I had during my master’s project. He suggested looking for molecules that could inhibit the coronavirus. It was a timely and meaningful project.”

How to trick a virus

Rijpkema focused on a specific part of the coronavirus: an enzyme that suppresses the immune system. Normally, the immune system responds to a virus by releasing signaling molecules that “raise the alarm” in the body. But this viral enzyme—called Mac1—removes part of such a signaling molecule, disrupting the signal and making it harder for the immune system to detect the infection.

The solution was to mislead the enzyme. “We make molecules that resemble the part of the signaling molecule that Mac1 normally binds to. But our molecules bind much more strongly. In this way, we keep the enzyme busy with decoy molecules, so it can no longer bind to the real signaling molecules.” This allows the immune system to respond more effectively to the virus.

From scattered puzzle pieces to one strong molecule

But how do you actually design a molecule that fits? In this case, Rijpkema could not rely on computer models. “We did try,” he says, “but so little was known about the enzyme at the time that the models did not give any clear direction.”

Instead, it came down to trial and error. For each part of the molecule, Rijpkema and his colleagues had to design a synthetic route: a series of chemical reactions starting from simple building blocks that together produce the desired molecule.

They then tested whether it worked, and adjusted it if it didn’t. “For the first two years, I basically only did things that didn’t work.” But this process helped him discover which changes improved the molecule. “In the end, we combined all the successful parts into one so-called ‘super molecule’ that binds very strongly to the enzyme.”

‘Another group just beat us to it’

Alongside challenging research, Rijpkema also faced tough competition. Just as he was ready to publish his first results, another study with similar findings appeared. “After two and a half years, we finally had something that worked, and then another group just beat us to it,” he says.

Rather than giving up, the team shifted their focus. “We emphasized not the biological data, but the way we had made our molecules,” he explains. “That was slightly different and more elegant than what the other group had done. It was a good learning moment. This is sometimes how science goes, but you have to be flexible and keep going.”

Decoy molecule as a stepping stone toward new medicine

The new decoy molecule is not a medicine in itself, but it is an important step forward. The molecules Rijpkema developed mainly help scientists better understand how the enzyme works.

That knowledge is crucial for pharmaceutical companies, which can use it to develop real treatments in the future. “We do fundamental research,” Rijpkema says. “But without that foundation, you cannot develop targeted medicines.”

Rijpkema will defend his Ph.D. thesis, “Synthesis of ADP-ribose Analogues,” on April 16. His supervisors are Dr. Dmitri Filippov and Professor Jeroen Codée.

Cancer cells excel at evading detection, but subtle chemical differences set them apart from healthy cells. Now, a team of scientists from Wageningen University & Research and Van Andel Institute has identified a way to exploit this distinction. Using a variant of CRISPR, a modern tool for editing DNA, they distinguished tumor DNA from healthy DNA and selectively cut only the former.

The study, published in Nature, is an early but promising step toward a cancer therapy that targets and destroys tumor cells with high precision.

The new method relies on methyl groups, small chemical tags attached to DNA that regulate whether genes are on or off. This process, called DNA methylation, is altered in cancer cells and can act as a molecular “fingerprint” that differentiates malignant cells from healthy ones.

Precision gene editing with ThermoCas9

The team conducted the study using ThermoCas9, a CRISPR variant discovered in bacteria several years ago by Wageningen’s John van der Oost, Ph.D. Like other CRISPR systems, researchers can program ThermoCas9 to locate and cut specific sections of DNA within a cell.

VAI’s Hong Li, Ph.D., and her lab analyzed ThermoCas9’s structure and found that it can distinguish between unmethylated and methylated genes.

The team then introduced ThermoCas9 into human cells grown in culture dishes: healthy cells in one set of dishes and tumor cells in another set of dishes. This approach worked: ThermoCas9 cut DNA in tumor cells while leaving healthy DNA intact. The system therefore proved capable of detecting the subtle chemical differences between healthy and tumor cells and acting on them.

“ThermoCas9 is the first CRISPR-associated enzyme to respond to differences in the most abundant type of DNA methylation in human and other eukaryotic cells,” Van der Oost said. “This means we now have a system that we can target specifically toward tumor cells.”

The study represents the first time a CRISPR-based method has relied on methylation to target human cancer cells.

“ThermoCas9 uses methylation like an address to precisely target cancer cells while leaving healthy cells untouched,” Li said. “The findings could be a game changer.”

A precise molecular fit

The explanation for ThermoCas9’s selective behavior lies in the way it binds to DNA. Before a CRISPR system cuts DNA, it must first attach to a short recognition sequence next to its target, known as the PAM (Protospacer Adjacent Motif). ThermoCas9 is unique in that its PAM sequence includes a human methylation site, meaning it can contain a methyl group.

“The CRISPR system binds very precisely to this recognition code,” Van der Oost explained.

Compare it to a screwdriver that fits perfectly into a matching screw head. If there is a protrusion inside the groove, the screwdriver no longer fits, nor is it capable of performing its job. In the same way, a methyl group disrupts the fit between ThermoCas9 and the DNA, preventing binding and leaving the DNA sequence untouched.

“ThermoCas9 is a perfect example of the value of fundamental research; you have to know how these individual pieces work together,” Li said. “We used biochemistry and structural biology to discover a mechanism that we one day hope will lead to more precise, effective cancer treatment.”

Steps toward clinical research

There is still a long way to go before the technology can be translated into a potential cancer treatment. The new study demonstrates selective DNA cleavage but does not yet show that this effect can kill tumor cells. The next step focuses on damaging tumor DNA sufficiently to trigger cell death.

Aberrant methylation patterns also play a role in many other diseases, including childhood cancers such as neuroblastoma and autoimmune disorders. In the future, ThermoCas9 or a similar CRISPR tool may evolve into a versatile molecular strategy that recognizes diseased cells by their chemical “signature” and selectively disables them.

A new analytical method could improve how cancer treatments are designed—by allowing scientists to track, for the first time, exactly where inside a living cell a drug accumulates. Researchers from the University of Surrey and King’s College London developed the method, which detects trace amounts of metal inside individual living cells and their internal compartments without the need to kill the cells first.

Published in Spectrochimica Acta Part B: Atomic Spectroscopy, the study looked at a class of cancer therapy called targeted radionuclide therapy. This works by attaching a radioactive particle to a molecule that seeks out tumor cells, delivering radiation directly to the cancer. Where inside the cell the drug ends up is critical. A drug that reaches the nucleus causes damage to cancer by targeting DNA. Until now, there was no reliable way to measure this in living cells.

Dr. Monica Felipe-Sotelo, senior lecturer in radiochemistry and analytical chemistry, co-author of the study from the University of Surrey, said, “We developed this method using two specialist facilities—the SEISMIC facility at King’s College London and the University of Surrey’s ICP-MS facility. Together, they allowed us to combine the cell-sampling and metal-detection steps in a single workflow for the first time. That combination is what makes it possible to ask not just whether a drug gets into a cell, but precisely where it goes once it’s there.”

The team used tiny glass capillary tips—10 micrometers wide for whole cells, 3 micrometers for subcellular structures—to extract individual living pancreatic cancer cells and material from within them, including mitochondria, under a microscope.

The SEISMIC facility at King’s, a specialist system for extracting material from single living cells, provided the sampling capability. Surrey’s laser ablation inductively coupled plasma mass spectrometry (ICP-MS) facility then enabled detection and measurement of thallium present using LA-ICP-MS—a technique that uses a laser to vaporize minute quantities of material before a mass spectrometer identifies and quantifies the metals within. The combination of capillary sampling at the sub-cellular level and LA-ICP-MS has not been performed before.

The researchers used thallium chloride as a chemically stable stand-in for thallium-201, a radioactive isotope under investigation as a cancer treatment candidate. Thallium was successfully detected in individual cancer cells and, for the first time, inside mitochondria-enriched material extracted from those cells, at extremely low amounts.

Dr. Claire Davison from King’s College London, said, “Thallium-201 is exciting as a potential cancer therapy precisely because its radiation acts over such a short distance—which means it could destroy tumor cells while sparing the healthy tissue around them. But that precision cuts both ways: the drug has to end up in the right part of the cell to do its job. This method gives us, for the first time, a way to find that out in living cells, and that is a significant step towards making this type of therapy work in practice.”

Dr. Dany Beste, senior lecturer in microbial metabolism from the University of Surrey, said, “The potential here goes well beyond cancer. Metals play important roles in a wide range of diseases—from infectious disease to diabetes and liver conditions—and we have few tools for studying exactly where they are accumulating within cells. This methodology gives us a way to do that with a level of precision and in conditions that are much closer to biological reality. That opens up a lot of questions we could not previously ask.”

Professor Melanie Bailey from King’s College London said, “We are continuing to develop this methodology at the SEISMIC facility and working with various different users to determine precisely where other drugs go when they enter cells, and what they do when they get there.”

The technique could be extended beyond cancer research to study how any metal-based drug or toxic substance distributes inside living cells. The team identified the extraction of additional cellular compartments—including the nucleus, where radiation damage to DNA occurs—as a key next step. Improving methods to verify the purity of the extracted subcellular material is also identified as a priority for future development.

Nutrients recovered from animal and human waste could drastically reduce synthetic fertilizer use in the U.S., according to a new Cornell University study that takes into account real-world implementation challenges like processing and transport.

In the study in Nature Sustainability, researchers found that animal and human waste in the U.S. could theoretically meet 102% of nitrogen and 50% of phosphorus needs for the nation’s agriculture, a value of more than $5.7 billion annually. But they also identified a major hurdle: a frequent mismatch between the location of the waste—often in areas densely populated with people or livestock—and agricultural regions with the highest fertilizer needs.

Still, by mapping and analyzing the sources of waste and of agricultural need, the research team found that large percentages of recoverable nutrients—37% of nitrogen and 46% of phosphorus—can be used locally, and more than half of the surplus nutrients can be redistributed to nearby regions with low economic and environmental costs.

“This is a coordination problem, not a resource problem,” said corresponding author and assistant professor Chuan Liao. “Even considering the real-world constraints, there’s still a substantial amount of nutrients that can be economically redistributed to meet crop needs.”

The research provides a blueprint for harnessing the vast, untapped potential of animal and human waste to reduce the U.S.’s reliance on synthetic fertilizers, which are energy-intensive to produce, harmful to the environment and often made overseas.

“Excessive use of synthetic fertilizers leads to water pollution, and the production itself generates more emissions—it’s a very intensive process,” Liao said. “And you can see with the Iran War, there are supply-chain issues that can lead to great food insecurity as well.”

Using publicly available data, the researchers mapped potential sources of human and animal waste as well as the need for nutrients across 15 major crops, at a resolution of around 10 kilometers.

Nutrient surpluses occurred in population-dense areas and livestock-intensive regions, such as the Northeast and parts of the West respectively, while deficits persisted in the Midwest and southern Great Plains. The researchers then analyzed the potential for redistributing nutrients, given the costs of both processing and transportation.

The team found that areas of very high or very low nutrient supply often overlapped with poorer counties, where people are more vulnerable to food insecurity and have worse overall health outcomes. Liao said pollution could be a factor: In surplus regions, more waste washes into bodies of water, and in areas of low-nutrient supply, farmers rely more on synthetic fertilizers, which can degrade soil and pollute water as well.

“The nutrient inequality seems to mirror social inequality in a large sense,” Liao said. “So potentially fixing the nutrient flow can promote environmental justice.”

Liao said the best approach to scale the use of waste in U.S. agriculture is to take advantage of opportunities at the local level. He gave the example of a pig farm in the middle of miles of corn fields: With the right infrastructure and incentives, waste from the pig farm could be used to satisfy the nutrient-hungry corn fields right next door.

“We’re advocating for a decentralized system, so that waste can be processed locally,” Liao said. “But in order to do this, we need to coordinate across different sectors, such as agriculture, waste and energy. The technology is there, but we need governance and infrastructure to scale up to the entire U.S.”

The study is part of a larger research program exploring the feasibility of using human and animal waste as fertilizer globally, with co-authors Rebecca Nelson, professor in CALS’ School of Integrative Plant Science (SIPS), and Johannes Lehmann, the Liberty Hyde Bailey Professor at SIPS.

An international team led by researchers at QUT has used artificial intelligence to create tiny “smart” proteins that switch on only when they detect a chosen target. Published in Nature Biotechnology, the research opens the way to a new generation of low-cost biosensors for medicine, environmental monitoring and biotechnology.

The team showed that these AI-designed protein switches could work inside living bacterial cells and could also be linked to electrodes to generate an electrical signal, similar in principle to glucose meters.

Lead author Professor Kirill Alexandrov, from the QUT School of Biology and Environmental Science and the ARC Centre of Excellence in Synthetic Biology, explained that proteins are the molecular machines that allow living cells to sense changes in their environment and respond.

“One of the major goals of synthetic biology is to build protein systems that can detect molecules of interest and then trigger a useful response,” Professor Alexandrov said. “Until recently, protein engineers were mostly limited to adapting natural proteins found in biology. That gave us only a small set of starting options and made it very difficult to design new sensors on demand. Our study shows that AI-designed proteins can be turned into effective molecular switches, greatly expanding what protein engineers can build.”

The researchers used machine learning-designed binding proteins as artificial receptors and connected them to enzymes capable of producing easily measurable outputs. These outputs included color changes, light emission and electrical signals, making the switches suitable for different types of sensing technologies.

Importantly, the work also challenges a long-held idea in protein science.

“It was widely believed that sensing proteins had to undergo large shape changes to function as switches,” Professor Alexandrov said. “We found that these artificial receptors do not need a dramatic structural rearrangement. Instead, binding of the target molecule subtly changes how the protein moves, and that is enough to turn activity on. That gives us new insight into how natural protein regulation works and provides a powerful new strategy for designing useful biosensors.”

In the study, the team built switches that responded to small molecules, peptides and proteins. They also demonstrated electrochemical biosensors for steroid detection and showed that the switches could operate in living cells, an important step towards future synthetic biology applications.

The technology could eventually support portable diagnostic devices, environmental sensing systems and engineered cells that respond intelligently to chemical signals.

The work brought together researchers from seven teams across Australia, the United Kingdom and the United States, including collaborators from the University of Washington led by 2024 Nobel Prize laureate Professor David Baker, and CSIRO, Australia’s national science agency.