Electricity-generating bacteria may power future innovations
Researchers uncover surprising survival strategy that could reshape biotech and energy systems
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Researchers including Caroline Ajo-Franklin and Biki Bapi Kundu have discovered how certain bacteria breathe by generating electricity.
view moreCredit: Photo by Jeff Fitlow/Rice University.
A team led by Rice University bioscientist Caroline Ajo-Franklin has discovered how certain bacteria breathe by generating electricity, using a natural process that pushes electrons into their surroundings instead of breathing on oxygen. The findings, published in Cell last month, could enable new developments in clean energy and industrial biotechnology.
By identifying how these bacteria expel electrons externally, the researchers offer a glimpse into a previously hidden strategy of bacterial life. This work, which merges biology with electrochemistry, lays the groundwork for future technologies that harness the unique capabilities of these microscopic organisms.
“Our research not only solves a long-standing scientific mystery, but it also points to a new and potentially widespread survival strategy in nature,” said Ajo-Franklin, professor of biosciences, director of the Rice Synthetic Biology Institute and a Cancer Prevention and Research Institute of Texas (CPRIT) Scholar.
Electric respiration explained
Most modern organisms rely on oxygen to metabolize food and release energy. Oxygen serves as the final electron acceptor in a chain of reactions that produces energy. But bacteria, far older than modern organisms such as humans and plants, have evolved other ways to respire in oxygen-deprived environments, including deep-sea vents and the human gut.
The researchers found that some bacteria use naturally occurring compounds called naphthoquinones to transfer electrons to external surfaces. This process, known as extracellular respiration, mimics how batteries discharge electric current, enabling bacteria to thrive without oxygen.
Scientists have long observed this unusual mode of respiration and harnessed it in biotechnology as something of a black box. Now, a Rice-led team has uncovered its mechanism — a breakthrough that suggests extracellular respiration may be far more common in nature than previously believed.
“This newly discovered mechanism of respiration is a simple and ingenious way to get the job done,” said Biki Bapi Kundu, a Rice doctoral student and first author of the study. “Naphthoquinones act like molecular couriers, carrying electrons out of the cell so the bacteria can break down food and generate energy.”
Simulating life without air
The Rice researchers partnered with the Palsson lab at the University of California San Diego to test their findings. Using advanced computer modeling, they simulated bacterial growth in environments devoid of oxygen but rich in conductive surfaces.
The simulations revealed that bacteria could indeed sustain themselves by discharging electrons externally. Further laboratory tests confirmed that bacteria placed on conductive materials continued to grow and generate electricity, effectively breathing through the surface.
This interdisciplinary approach deepened the understanding of bacterial metabolism’s versatility and revealed a real-time method for electronically monitoring and influencing bacterial behavior.
Applications in clean technology and beyond
This foundational discovery has far-reaching practical implications. Biotechnology processes such as wastewater treatment and biomanufacturing could be significantly improved through better management of electron imbalances. Electricity-exhaling bacteria could fix these imbalances to keep the systems running efficiently.
“Our work lays the foundation for harnessing carbon dioxide through renewable electricity, where bacteria function similarly to plants with sunlight in photosynthesis,” Ajo-Franklin said. “It opens the door to building smarter, more sustainable technologies with biology at the core.”
The technology may also enable bioelectronic sensors in oxygen-deprived environments, offering new tools for medical diagnostics, pollution monitoring and deep-space exploration.
Co-authors of this study include Jayanth Krishnan, Richard Szubin, Arjun Patel, Bernhard Palsson and Daniel Zielinski of UC San Diego. CPRIT and the Novo Nordisk Foundation funded the study.
Journal
Cell
Article Title
Extracellular respiration is a latent energy metabolism in Escherichia coli
Ultimate self-sacrifice: Bacteria activate unusual defense to evade viral attack
Scientists discover that a well-known defense system in some bacteria can kill the cell as a last resort if viruses try to thwart it
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Sukrit Silas and his colleagues at Gladstone Institutes and UC San Francisco discovered that a well-known defense system in some bacteria can kill the cell as a last resort if viruses try to thwart it.
view moreCredit: Michael Short/Gladstone Institutes
SAN FRANCISCO—For billions of years, viruses and bacteria have been embroiled in an arms race. In response to constant attacks by viruses known as bacteriophages—more commonly called “phages”—bacteria evolve new ways to defend themselves. And, in turn, phages evolve new strategies to overcome those defenses.
Now, in a study published in Molecular Cell, scientists at Gladstone Institutes and UC San Francisco (UCSF) have uncovered new details about this ongoing warfare related to an unexpected response among certain bacterial cells: self-destruction. The findings could be useful for developing novel antibiotics or treatments for drug-resistant infections.
The study deals with the most widespread antiviral defense in bacteria, a mechanism known as the “restriction modification” system. This defense system detects DNA from an invading phage and cuts it into pieces before the phage can take over the cell.
But some phages have developed counter-defenses that inhibit this system, allowing them to sneak in. The scientists observed that if bacterial cells sense this counter-defense, they trigger their own death using components of the very same systems that the phages were trying to inhibit.
“We think this is essentially the first and second lines of defense merged into one,” says Gladstone Investigator Sukrit Silas, PhD, lead author of the study. “You could say it’s the bacterial immune system deciding the infection has gone too far and altruistically initiating its own destruction or dormancy so the phage cannot replicate. This protects neighboring bacterial cells from becoming infected.”
Overlooked Genes Hold Special Powers
Silas and his colleagues made their discovery while trying to better understand underexplored parts of phage genomes known as accessory regions. The genes in these regions aren’t always essential for the phage’s survival, but may be necessary in certain circumstances, such as helping them escape detection by bacterial immune systems.
Because accessory genes in phages are non-essential, they are often overlooked and most have yet to be identified; a big part of Silas’ research at Gladstone is focused on filling this enormous knowledge gap.
“There are probably at least tens of thousands of these genes scattered all across phage genomes,” says Silas, who’s also an assistant professor in the Department of Microbiology and Immunology at UCSF. “Given that the few that have been previously explored often turn out to be counter-defense genes, I became very curious in finding more and learning what they do.”
Traditional methods of studying accessory genes can only manage a handful of genes at a time. So, the researchers designed a new research platform with a more efficient algorithm that can study thousands of accessory genes at once for any phage genome family.
Using the new platform, Silas and his colleagues identified more than 10,000 novel accessory genes in more than 1,000 genomes of phages that infect bacteria in the Enterobacteria family, which includes E. coli. They took a closer look at 200 of these new genes by turning them on and off in different strains of E. coli to explore their effects.
Forcing Phages into a Trap
Some accessory genes neutralized bacterial restriction-modification systems, allowing phages to infect cells. However, some of the genes instead triggered bacterial cells in some strains of E. coli to self-destruct. In fact, the researchers found that multiple different phage accessory genes can trigger the same path to initiate cell death.
When they looked to see what defenses in the bacteria were responsible for this self-killing, they were surprised to find systems derived from the bacterial restriction-modification system itself.
“The bacteria’s defense system can detect if the phage is trying to block it, and in response, the bacterial cell destroys itself from within,” Silas says. “It’s pretty remarkable that a system we’ve known about for so long can have this property we weren’t aware of.”
“Our study expands our understanding of the evolutionary arms race between bacteria and phages,” says Joe Bondy-Denomy, PhD, of UCSF, who co-led the study with Silas. “These cell-killing responses seem to be evolutionary traps for phages; having these accessory genes may run the risk of triggering the death of the cells they’re trying to infect. But losing the same genes could make phages vulnerable to the destruction of their own DNA.”
New Opportunities for Discovery
The research platform developed for this study could accelerate the understanding of thousands of additional accessory genes in phages that infect a wide range of microbial species.
By illuminating specific tactics, vulnerabilities, and trends in the bacteria-phage arms race, this work could inform efforts to design novel antimicrobial treatments and fight drug-resistant bacteria.
“I’m an evolutionary biologist at heart, but the time that I’ve spent at Gladstone has been transformative in terms of how I think about my research,” Silas says. “I’m not just asking what these genes do, but using that information to home in on what matters most to certain phages and bacteria, and what we would need to understand to design a novel treatment that could make it into a clinical trial.”
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About the Study
The paper “Activation of bacterial programmed cell death by phage inhibitors of host immunity,” was published in the journal Molecular Cell on May 1, 2025.
In addition to Sukrit Silas and Joe Bondy-Denomy, the study’s other authors are Héloïse Carion, Eric S. Laderman, and Matthew Johnson from UCSF; Kira S. Makarova and Eugene V. Koonin from the National Institutes of Health; Thomas Todeschini and Franklin L. Nobrega from the University of Southampton; Pradeep Kumar from ONI; and Michael Bocek from Twist Biosciences.
The work was supported by the Damon Runyon Fellowship Award (DRG 2352-19), the Vallee Foundation, the Searle Scholars Program, the Kleberg Foundation, and the U.S. Department of Health and Human Services (National Institutes of Health and National Library of Medicine).
About Gladstone Institutes
Gladstone Institutes is an independent, nonprofit life science research organization that uses visionary science and technology to overcome disease. Established in 1979, it is located in the epicenter of biomedical and technological innovation, in the Mission Bay neighborhood of San Francisco. Gladstone has created a research model that disrupts how science is done, funds big ideas, and attracts the brightest minds.
Journal
Molecular Cell
Article Title
Activation of bacterial programmed cell death by phage inhibitors of host immunity
Article Publication Date
1-May-2025
