UC Riverside scientists have now discovered a chemical that plants produce when they’re stressed prevents biofilm from forming. The breakthrough offers potential advances in healthcare as well as preventing equipment corrosion in industrial settings.

“In simple terms, biofilms are communities of microorganisms, like bacteria or fungi, that stick together and form a protective layer on surfaces,” said Katayoon Dehesh, distinguished professor of molecular biochemistry at UCR, and corresponding author of a study about the discovery.

“You’ve probably seen them as the slimy layer on river rocks or the plaque on your teeth. While they’re a natural part of many ecosystems, biofilms can cause big problems.”

The study, published in the journal Nature Communications, highlights the importance of a particular metabolite, which is a molecule produced during life-sustaining chemical reactions inside plants, as well as bacteria and even some parasites, like the one that causes malaria.

In plants, this metabolite, MEcPP, plays a critical role not only in producing essential compounds but also in stress signaling. For example, when a plant is damaged in some way and too much oxygen enters its cells, it accumulates MEcPP. This molecule then triggers protective responses within the plant. The researchers discovered that this same molecule has a surprising effect on bacteria like E. coli: it disrupts biofilm development by interfering with its ability to attach to surfaces.

In medical settings, biofilms grow on devices like catheters, stents, or implants, making infections harder to treat because the microbes in biofilms are highly resistant to antibiotics. In industrial contexts, they clog pipes, contaminate food processing equipment, and cause corrosion.

“By preventing the early stages of biofilm development, this molecule offers real potential to improve outcomes in any industries reliant on clean surfaces,” Dehesh said.

Bacteria rely on hair-like structures called fimbriae to anchor themselves to surfaces, a critical step in biofilm initiation. Fimbriae help bacteria latch onto medical implants, pipes, or even teeth, where they secrete a protective matrix that shields them from antibiotics and cleaning agents. Without fimbriae, biofilm formation cannot begin.

“Biofilms are like fortresses for bacteria,” said Jingzhe Guo, UCR project scientist and first author of the paper. “By disrupting the initial phase of attachment, MEcPP essentially disarms the bacteria’s ability to establish these fortresses.”

Through genetic screenings of more than 9,000 bacterial mutants, the research team identified a key gene called fimE, which acts as an “off switch” for fimbriae production. MEcPP enhances the activity of this gene and increases the expression of fimE. This, in turn, prevents the bacteria from producing fimbriae and forming biofilms.

“Our discovery could inspire biofilm prevention strategies across a wide range of industries,” Guo said. “From cleaner water systems to better dental care products, the possibilities are immense.”

Biofilms are not only a medical concern but also a costly problem in industrial settings. They contribute to clogged pipelines, corroded machinery, and contamination in food processing facilities. Traditional methods for managing biofilms often rely on harsh chemicals or expensive treatments, which can be harmful to the environment or ineffective over time as bacteria adapt.

“This study is a testament to the unexpected connections between plant biology and microbiology,” Guo said. “It’s thrilling to think a molecule that plants use to signal stress might one day help humans combat bacterial threats.”

While previous research focused on how well organic solar cells converted light to electricity following radiation exposure, the new investigation also dug into what happens at the molecular level to cause drops in performance.

“Silicon semiconductors aren’t stable in space because of proton irradiation coming from the sun,” said Yongxi Li, first author of the study to be published in Joule and a U-M associate research scientist in electrical and computer engineering at the time of the research. “We tested organic photovoltaics with protons because they are considered the most damaging particles in space for electronic materials.”

Space missions often land on gallium arsenide for its high efficiency and resistance to damage from protons, but it’s expensive and, like silicon, is relatively heavy and inflexible. In contrast, organic solar cells can be flexible and are much lighter. This study is among those exploring the reliability of organics, as space missions tend to use highly trusted materials.

Organic solar cells made with small molecules didn’t seem to have any trouble with protons — they showed no damage after three years worth of radiation. In contrast, those made with polymers — more complex molecules with branching structures — lost half of their efficiency.

“We found that protons cleave some of the side chains, and that leaves an electron trap that degrades solar cell performance,” said Stephen Forrest, the Peter A. Franken Distinguished University Professor of Engineering at U-M, and lead corresponding author of the study.

These traps grab onto electrons freed by light hitting the cell, preventing them from flowing to the electrodes that harvest the electricity.

“You can heal this by thermal annealing, or heating the solar cell. But we might find ways to fill the traps with other atoms, eliminating this problem,” Forrest said.

It’s plausible that sun-facing solar cells could essentially self-heal at temperatures of 100°C (212°F) — this warmth is enough to repair the bonds in the lab. But questions remain: for instance, will that repair still take place in the vacuum of space? Is the healing reliable enough for long missions? It may be more straightforward to design the material so that the performance-killing electron traps never appear.

Li intends to explore both avenues further as an incoming associate professor of advanced materials and manufacturing at Nanjing University in China.

The research is funded by Universal Display Corp and the U.S. Office of Naval Research.

The devices were built in part at the Lurie Nanofabrication Facility, exposed to a proton beam at the Michigan Ion Beam Laboratory, and studied at the Michigan Center for Materials Characterization.

The team has applied for patent protection with the assistance of U-M Innovation Partnerships. Universal Display has licensed the technology from U-M and filed a patent application. Forrest has a financial interest in Universal Display Corp.

Plant scientists from the University of Nottingham, in collaboration with Shanghai Jiao Tong University, have identified how abscisic acid (ABA), a plant hormone known for its role in drought response, influences root growth angles in cereal crops such as rice and maize. The results have been published in Current Biology.

The study highlights how ABA and auxin, another key hormone, work together to shape root growth angle, providing a potential strategy to develop drought-resistant crops with improved root system architecture.

Drought poses a major threat to global food security, and enhancing the ability of crops to withstand water shortages is crucial. Drought, a major abiotic stressor, has caused substantial crop production losses of approximately $30 billion over the past decade. With a projected population of 10 billion by 2050 and serious freshwater depletion, developing drought-resistant crops is of paramount importance

Plants rely on their root systems, the primary organs for interacting with soil, to actively seek water. In drought conditions, water often depletes in the topsoil and remains accessible only in the deeper subsoil layers. Abscisic acid (ABA) plays an important role in helping plants adapt to these challenging conditions. This new study gives new insights into how ABA changes root growth angles to enable plants to reach out deeper subsoils in search of water.

The researchers discovered a new mechanism where ABA promotes the production of auxin, which enhances root gravitropism to grow them at steeper angles in response to drought. Experiments showed that plants with genetic mutations that block ABA production had shallower root angles and weaker root bending response to gravity compared to normal plants. These defects were linked to lower auxin levels in their roots. By adding auxin externally, the researchers restored normal root growth in these mutants, showing that auxin is key to this process.

The findings were consistent across both rice and maize, suggesting that this mechanism could apply to other cereal crops as well.

Dr Rahul Bhosal, Assistant Professor from the School of Bioscience is one of the lead authors on the study, he said: “Finding ways to tackle food insecurity is vital and the more we understand the mechanisms that control plant growth, the closer we are to designing systems to help plants to do this and improve crop yields during droughts.”

“Criteria for better identifying DLB exists in research settings, but we wanted to pull research studies together to establish something applicable for clinical settings,” says Ece Bayram, MD, PhD, assistant professor of neurology at the University of Colorado Anschutz Medical Campus and study lead author. “By pooling information from available publications, we were able to establish a cognitive profile that can differentiate DLB from Alzheimer’s before the dementia stage hits, which could better help inform the direction of care for people with these diseases.”

Researchers were able to identify consistencies in cognitive symptoms among people with DLB compared to people with Alzheimer’s in a meta-analysis of pre-dementia stage diagnoses. At the pre-dementia stage, people with DLB demonstrated more diminished attention, processing speed and executive function as well as better immediate recall and memory compared to people with Alzheimer’s.

“Identifying cognitive profiles gave us the outcome necessary to suggest guidelines that practitioners could easily be trained in to better tailor plans of care,” says Bayram. “Furthermore, providing framework for clinical assessment versus biomarker testing means more accessibility for practitioners. It is easier and cheaper to train in providing cognitive assessments than administering imaging or invasive biomarker tests,” says Bayram.

Researchers say identifying the form of dementia early can guide future planning for both the person with dementia and their care partners, and ease disease by providing proper symptomatic treatment. People with DLB, for instance, are reactive to certain types of commonly prescribed medications for psychosis, such as haloperidol, that tend to worsen their condition. Dr. Bayram says, overall, this study provides a promising step in advancing dementia prevention and care.

“We are seeing more and more treatment trials that are focused on disease modification for both Alzheimer’s and Lewy body diseases. Having validated clinical criteria to diagnose DLB before dementia hits means we can prevent it from happening instead of reacting to it after significant loss in the brain has occurred. These types of clinical assessments provide opportunities for everyone to receive care even without access to a specialty center.”

In this study, researchers aimed to understand how CAR T cells with different signaling domains work at the molecular and cellular levels to lay the foundation for designing CAR molecules that maximize antitumor activity beyond B cell malignancies.

“We looked at two different types of CAR T cells. The first, CD28.ζ-CART cells, are like sprinters. They kill cancer cells quickly and efficiently, but their activity is short-lived. The second, 4-1BB.ζ-CART cells, are like marathon runners. They kill cancer cells consistently over a long period,” said senior author Dr. Nabil Ahmed, professor of pediatrics — hematology and oncology at Baylor and Texas Children’s. “We need to understand what’s happening at the molecular level so we can engineer CAR T cells to adapt their killing behavior to target hard-to-treat malignancies, such as solid tumors.” Ahmed also is a member of the Center for Cell and Gene Therapy and the Dan L Duncan Comprehensive Cancer Center.

Led by first author Dr. Ahmed Gad, postdoctoral associate in Ahmed’s lab, the research team examined molecular dynamics at the immune synapse. The team biopsied the CAR T cell immunological synapse by isolating the membrane lipid rafts — cholesterol-rich molecules on the cell surface where most molecular interactions between cells take place.

They found that CD28.ζ-CAR molecules shuttle through the immune synapse quickly, working within minutes to kill cancer cells. This enabled fast CAR T cell recovery and a mastery of “serial killing” of cancer cells. In contrast, researchers found that 4-1BB.ζ-CAR molecules linger in the lipid rafts and immune synapse. The 4-1BB.ζ-CAR T cells multiply and work together, resulting in sustained “collaborative” killing of tumor cells.

“Observing the distinct pattern of dynamics between single molecules helps us understand the big picture of how these products work,” Gad said. “Next, we are studying how to dynamically adapt these CAR T cells at the synapse level to make them more effective.”

“Tumors are very sophisticated. We need to adapt our tools to the biology of the disease. This may involve using multiple tools that work in different ways at different stages,” Ahmed added.

Other authors who contributed to this work include Jessica S. Morris, Lea Godret-Miertschin, Melisa J. Montalvo, Sybrina S. Kerr, Harrison Berger, Jessica C.H. Lee, Amr M. Saadeldin, Mohammad Abu-Arja, Shuo Xu, Spyridoula Vasileiou, Rebecca M. Brock, Kristen Fousek, Mohamed F. Sheha, Madhuwanti Srinivasan, Yongshuai Li, Arash Saeedi, Kandice Levental, Ann M. Leen, Maksim Mamonkin, Alexandre Carisey, Navin Varadarajan, Meenakshi Hegde, Sujith K. Joseph, Ilya Levental and Malini Mukherjee. They are affiliated with one or more of the following institutions: Baylor College of Medicine, Texas Children’s Hospital, Center for Cell and Gene Therapy, the Dan L Duncan Comprehensive Cancer Center, the University of Houston, and the University of Virginia.

This work was supported by the National Institutes of Health U54 Moonshot Grant, the National Cancer Institute, the Cancer Prevention and Research Institute of Texas, the Be Brooks Brave Fund St. Baldrick’s Foundation Fellowship, Stand Up To Cancer, the St. Baldrick’s Pediatric Cancer Dream Team Translational Research Grant, Triumph Over Kids Cancer Foundation, the Alex Moll Family Fund, and The Faris Foundation.