Study in mice shows potential for gene-editing to tackle mitochondrial disorders

Mitochondria - 3D illustration 
Credit: wir0man/Getty Images

Our cells contain mitochondria, which provide the energy for our cells to function. Each of these mitochondria contains a tiny amount of mitochondrial DNA. Mitochondrial DNA makes up only 0.1% of the overall human genome and is passed down exclusively from mother to child.

Faults in our mitochondrial DNA can affect how well the mitochondria operate, leading to mitochondrial diseases, serious and often fatal conditions that affect around 1 in 5,000 people. The diseases are incurable and largely untreatable.

There are typically around 1,000 copies of mitochondrial DNA in each cell, and the percentage of these that are damaged, or mutated, will determine whether a person will suffer from mitochondrial disease or not. Usually, more than 60% of the mitochondria in a cell need to be faulty for the disease to emerge, and the more defective mitochondria a person has, the more severe their disease will be. If the percentage of defective DNA could be reduced, the disease could potentially be treated.

A cell that contains a mixture of healthy and faulty mitochondrial DNA is described as ‘heteroplasmic’. If a cell contains no healthy mitochondrial DNA, it is ‘homoplasmic’.

In 2018, a team from the MRC Mitochondrial Biology Unit at the University of Cambridge applied an experimental gene therapy treatment in mice and were able to successfully target and eliminate the damaged mitochondrial DNA in heteroplasmic cells, allowing mitochondria with healthy DNA to take their place.

Delivery of antioxidants to liver mitochondria

Damage to the liver induced by acetaminophen (dotted blue outlines) is almost completely mitigated by CoQ10-MITO-Porter (right), compared to the effect of phosphate buffered saline (left) and direct administration of CoQ10(center).
Image Credit: Mitsue Hibino, et al. Scientific Reports. May 10, 2023

A new drug delivery system delivers an antioxidant directly to mitochondria in the liver, mitigating the effects of oxidative stress.

Mitochondria are microscopic organelles found within cells, and are well-known as the “powerhouse of the cell.” They are by far the largest producer of the molecule adenosine triphosphate (ATP), which provides energy to many processes in living cells. The process by which mitochondria synthesize ATP generates a large amount of reactive oxygen species (ROS), chemical groups that are highly reactive. 

In a healthy cell, the ROS is controlled by the mitochondria; however, when this balance is lost, the excess ROS damages the mitochondria and subsequently cells and tissues. This phenomenon, known as oxidative stress, can cause premature aging and disease. The ROS that causes oxidative stress can be controlled by antioxidants.

A research team led by Professor Yuma Yamada, Distinguished Professor Hideyoshi Harashima and Assistant Professor Mitsue Hibino at Hokkaido University have developed a system to deliver antioxidants to mitochondria to mitigate the effects of excess ROS. Their findings were published in Scientific Reports.

Discovery reveals fragile X syndrome begins developing even before birth

The energy-making organelles called mitochondria (shown in green) that work inside cells to make energy aren’t working as they should in the neurons (shown in red) of people with fragile X syndrome. UW–Madison researchers have identified a protein and gene involved in this mitochondrial dysfunction, as well as a potential treatment.
Image Credit: Minjie Shen

Fragile X syndrome, the most common form of inherited intellectual disability, may be unfolding in brain cells even before birth, despite typically going undiagnosed until age 3 or later.

A new study published today in the journal Neuron by researchers at the University of Wisconsin–Madison showed that FMRP, a protein deficient in individuals with fragile X syndrome, has a role in the function of mitochondria, part of a cell that produces energy, during prenatal development. Their results fundamentally change how scientists understand the developmental origins of fragile X syndrome and suggest a potential treatment for brain cells damaged by the dysfunction.

Xinyu Zhao is a neuroscience professor and neurodevelopmental diseases researcher at UW–Madison’s Waisman Center. Four postdoctoral fellows in her lab led the study.

Targeting mitochondria and related protein suggest new therapeutic strategy for treating Lou Gehrig's disease (ALS)

Researchers have discovered a receptor, sigma-1 receptor (green), and a protein, ATAD3A (red),  that are associated with Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig’s disease.
Image Credit: Yamanaka Laboratory

Researchers at Nagoya University in Japan have discovered a receptor, sigma-1 receptor, and a protein, ATAD3A, that are associated with Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig’s disease. Since there are drugs that specifically target the receptor, their findings suggest a new therapeutic strategy. They published the study in the journal Neurobiology of Disease. 

ALS causes degeneration of motor neurons and the resulting muscle atrophy. Some of this degeneration is the result of the dysfunction of mitochondria, the energy-generating organelles of the body. This dysfunction causes a lack of energy in neurons resulting in the characteristic symptoms of the disease.   

The integrity of the mitochondria-associated membrane (MAM) is important for the stability of the mitochondria. The MAM is especially important during the processes of division of mitochondria (called fission) and mitochondria fusing together (called fusion). Several proteins, including enzymes, are associated with these processes and accumulate in the MAM.  

What Is: Mitochondrion

Evolutionary Singularities and the Eukaryotic Dawn

The mitochondrion represents a biological singularity, a discrete evolutionary event that fundamentally partitioned life on Earth into two distinct energetic stratums: the prokaryotic and the eukaryotic. While colloquially reduced to the moniker of "cellular powerhouse," the mitochondrion is, in functional reality, a highly integrated endosymbiont that serves as the master regulator of eukaryotic physiology. It is the nexus of cellular respiration, the arbiter of programmed cell death, a buffer for intracellular calcium, and a hub for biosynthetic pathways ranging from heme synthesis to steroidogenesis. To comprehend the complexity of multicellular life, one must first dissect the intricate molecular sociology of this organelle.   

The origin of the mitochondrion is the subject of intense phylogenomic reconstruction. The prevailing consensus, the endosymbiotic theory, posits that the mitochondrion descends from a free-living bacterial ancestor—specifically a lineage within the Alphaproteobacteria—that entered into a symbiotic relationship with a host archaeal cell approximately 1.5 to 2 billion years ago. This was not a trivial acquisition but a transformative merger. The energetic capacity afforded by the internalization of a bioenergetic specialist allowed the host cell to escape the surface-area-to-volume constraints that limit prokaryotic genome size, facilitating the expansion of the nuclear genome and the development of complex intracellular compartmentalization. 

Chloroplast from the father

Tobacco seedlings on growth medium with an antibiotic. Plants with exclusively maternally inherited chloroplasts sensitive to the antibiotic are pale. Two seedlings contain green, intact chloroplasts in the leaves (red arrows). These chloroplasts are resistant to the antibiotic and were passed on from the father plant.
Image Credit: MPI-MP

Under cold conditions, not only the mother plant but also the father plant can pass on its chloroplasts to the offspring

Scientists at the Max Planck Institute of Molecular Plant Physiology in Potsdam (Germany) analyzed for the first time the inheritance of chloroplasts under a wide range of environmental conditions. Contrary to the prevailing view that chloroplasts are only passed on by the mother plant, paternal chloroplasts can also be transmitted to the offspring under cold conditions. Maternal and paternal chloroplasts thus meet in the offspring and may be able to exchange genetic material with each other. The new findings may allow plant breeders for the first time to selectively use traits from the genetic material of chloroplasts.

A story of flowers and bees is the classic introduction to a topic that is still discussed far too scarcely in our society: sex in plants! When plants reproduce, the sperms within the pollen grains fuse with the egg cell within the flower the pollen has landed on. In this way, the genetic material of the cell nuclei of both parents is combined in the seed. This is important, as it allows harmful mutations to be purged that otherwise would accumulate in the genetic material over generations.

Evolutionary Tuning of a Cellular “Powerhouse”

Profiles of the subunits of individual complexes (top) and overall representation of all around 5200 protein signals in MitCOM.
Image Source | Credit: AG Fackler/Pfanner/Becker

Mitochondria are membrane-enclosed structures found in all cells of higher organisms, where they produce most of the necessary energy (“powerhouses of the cell”). In addition, these organelles serve important functions in the synthesis and degradation of certain biomolecules as well as in numerous intercellular signaling processes. In close collaboration, a team of researchers led by Prof. Dr. Nikolaus Pfanner and Prof. Dr. Bernd Fakler from the University of Freiburg Institutes of Biochemistry and Physiology, respectively, and by Prof. Dr. Thomas Becker from the Institute of Biochemistry at the University of Bonn has now applied a newly developed analytical method to comprehensively map the structural organization of proteins in mitochondria. The results provide initial insight into the structure and organization of the mitochondrial proteins in protein machineries of varying complexity, thus laying the foundation for future studies of new protein functions and structures. This study was published in the journal Nature.

Comprehensive picture of the composition of protein complexes indispensable

Researchers discover new leukemia-killing compounds

Natasha Kirienko (left) and Svetlana Panina in Kirienko’s Rice University laboratory in 2019. Kirienko, associate professor of biosciences, and Panina, a former postdoctoral research associate in Kirienko’s lab, collaborated with researchers at the University of Texas MD Anderson Cancer Center to study potential new mitophagy-inducing drugs that could be paired with other chemotherapies to deliver a potent one-two punch to leukemia.
Photo by Jeff Fitlow/Rice University

Researchers from Rice University and the University of Texas MD Anderson Cancer Center have discovered potential new drugs that work in concert with other drugs to deliver a deadly one-two punch to leukemia.

The potential drugs are still years away from being tested in cancer patients, but a recently published study in the journal Leukemia highlights their promise and the innovative methods that led to their discovery.

In previous studies, the research groups of Rice biochemist Natasha Kirienko and MD Anderson physician-scientist Marina Konopleva screened some 45,000 small-molecule compounds to find a few that targeted mitochondria. In the new study, they chose eight of the most promising compounds, identified between five and 30 closely related analogs for each and conducted tens of thousands of tests to systematically determine how toxic each analog was to leukemia cells, both when administered individually or in combination with existing chemotherapy drugs like doxorubicin.

“One of the big challenges was to establish optimal conditions and doses for testing on both cancer cells and healthy cells,” said study lead author Svetlana Panina , a researcher at the University of Texas at Austin who conducted the research during her postdoctoral studies at Rice. “The results from our previously published cytotoxicity assay were helpful, but very little is known about these small-molecule compounds. None of them had been thoroughly described in other studies, and we had to essentially start from scratch to determine how much to use, what they do in cells, everything. All the doses and treatment conditions had to be adjusted by multiple preliminary experiments.”

Study untangles mitochondria to reap rewards of exercise

New research has uncovered how mitochondria – the energy powerhouse of our cells implicated in devastating mitochondrial disease, type 2 diabetes and cancers – respond to exercise training in unprecedented detail.

 joint study between the University of Melbourne and Victoria University, with collaborators at the German Diabetes Center, Monash University, and the Murdoch Children’s Research Institute, have successfully linked minutes of exercise to specific mitochondrial changes that support improved metabolism.

In work published in Nature Communications, the University of Melbourne’s Dr Stroud from the School of Biomedical Sciences, and colleagues detail how they used state-of-the art equipment at the University of Melbourne’s Bio21 Molecular Science and Biotechnology Institute’s Mass Spectrometry and Proteomics Faculty to analyze in detail how our muscles respond to exercise.

While mitochondria are hugely important as they convert sugars, fats and protein into energy used for muscle contraction, cell growth and brain activity among other things, maintaining mitochondrial health is critical not just to various debilitating disease states where mitochondrial function is impaired, but also the quality of life of otherwise healthy people.

The team were able to discover ten times more mitochondrial proteins that respond to exercise training than documented in previous studies.

How a Small Protein Plays a Large Role in Mitochondrial Function

Rebecca Voorhees
Credit: Caltech

Caltech researchers have discovered an unexpected role for a protein in human cells, solving a longstanding mystery about how the composition of mitochondrial membranes is regulated.

Multiple studies have previously shown that mutations in the protein MTCH2 are associated with a wide range of disorders such as Alzheimer's disease, Parkinson's disease, and leukemia, but it has been unclear what exactly MTCH2 was doing to have such a major effect on the cell's function. This new work shows that MTCH2 is critical for the construction of a cell's mitochondria, specifically for carefully inserting proteins into the mitochondrial outer membrane.

The research was conducted in the laboratory of Rebecca Voorhees, assistant professor of biology and biological engineering and a Heritage Medical Research Institute Investigator, and was a close collaboration with the laboratory of Jonathan Weissman at the Whitehead Institute at MIT. A paper describing the study appears in the journal Science on October 21.

Ancestral mitoviruses discovered in mycorrhizal fungi

Arbuscular mycorrhizal (AM) fungi in the Glomeromycotina colonize plant roots (left, micrograph) and deliver water and nutrients from soil (right).
Image Credit: Tatsuhiro Ezawa

A new group of mitochondrial viruses confined to the arbuscular mycorrhizal fungi Glomeromycotina may represent an ancestral lineage of mitoviruses.

Mitochondria are organelles in the cells of almost all eukaryotes — organisms with cells that have a nucleus. They were originally free-living bacteria capable of generating energy in the presence of oxygen; then engulfed by an ancestral eukaryotic cell where they became mitochondria, the site of cellular respiration and many important metabolic processes. In humans, dysfunctions of mitochondria are associated with aging and many diseases.

Bacteriophages are viruses that infect bacteria. As former bacteria, there are also viruses that infect mitochondria, known as mitoviruses, which evolved from bacteriophages. While mitoviruses have been found in fungi, plants, and invertebrates, they are not well studied.

Associate Professor Tatsuhiro Ezawa at Hokkaido University, Professor Luisa Lanfranco at University of Torino, and Dr. Massimo Turina at National Research Council of Italy (CNR) Torino led an international team to discover a new group of mitoviruses, called large duamitoviruses. Their findings were published in the journal mBio.

Origin of complex cells started without oxygen

Since the 1960s, many experts have argued that the emergence of eukaryotes (cells containing a clearly defined nucleus) happened in response to the oxygenation of Earth’s surface environment.

But a team led by the universities of Stanford and Exeter say recent advances in the Earth and life sciences challenge this view.

Their review says these breakthroughs "decouple" the emergence of eukaryotes (known as eukaryogenesis) from rising oxygen levels, and suggest eukaryotes in fact emerged in an anoxic (no-oxygen) environment in the ocean.

"We can now independently date eukaryogenesis and key oxygenation transitions in Earth history," said Dr Daniel Mills, of Stanford University.

"Based on fossil and biological records, the timing of eukaryogenesis does not correlate with these oxygen transitions in the atmosphere (2.22 billion years ago) or the deep ocean (0.5 billion years ago).

"Instead, mitochondria-bearing eukaryotes are consistently dated to between these two oxygenation events, during an interval of deep-sea anoxia and variable surface-water oxygenation."

The emergence of mitochondria – the energy-producing "powerhouses" of eukaryote cells – is now thought to be the defining step in eukaryogenesis.

Mitochondria have different DNA to the cells in which they live, and the new paper addresses the possible origin of this symbiotic relationship, famously championed by the biologist Lynn Margulis.

How heart failure disrupts the cell’s powerhouse

From left: Shingo Takada, Hokkaido University and Hokusho University; Shintaro Kinugawa, Kyushu University; and Hisataka Sabe, Hokkaido University
Photos credits: Shingo Takada, Shintaro Kinugawa, Hisataka Sabe

Chronic heart failure causes the cell’s powerhouses to dysfunction, in part due to overconsumption of an important intermediary compound in energy production. Supplementing the diet to compensate for this could prove a promising strategy for treating heart failure. The findings were published in the journal PNAS by Hokkaido University scientists and colleagues in Japan.

Mitochondria are small organelles found in almost every cell and are responsible for converting carbohydrates, fats and proteins into energy to power biochemical reactions. Chronic heart failure is known to be associated with mitochondrial dysfunction, but much is still unknown about how this happens at the molecular level.

A research team consisting of molecular biologist Hisataka Sabe (Hokkaido University), cardiovascular medicine specialists Shingo Takada (Hokkaido University and Hokusho University) and Shintaro Kinugawa (Kyushu University) and their colleagues studied the biochemical processes that occur in mice with chronic heart failure caused by surgically blocking part of the blood supply to their hearts. They specifically looked at heart cells outside the boundaries of dead tissue.

Researchers Show SARS-Cov-2 Infection Affects Energy Stores in the Body, Causing Organ Failure

Jonathan C. Schisler, PhD
Photo Credit: Courtesy of UNC

An international research team, including Jonathan C. Schisler, PhD, in the UNC School of Medicine, has found how SARS-CoV-2 causes widespread “energy outages” throughout major organs, and how these effects contribute to debilitating long COVID symptoms.

The lungs were once at the forefront of SARS-Cov-2 research, but as reports of organ failure and other serious complications poured in, scientists set out to discover how and why the respiratory virus was causing serious damage to the body’s major organs, including the lungs.

An interdisciplinary COVID-19 International Research Team (COV-IRT), which includes UNC School of Medicine’s Jonathan C. Schisler, PhD, found that SARS-CoV-2 alters mitochondria on a genetic level, leading to widespread “energy outages” throughout the body and its major organs. Their findings, published in Science Translational Medicine, explain how these effects contribute to long COVID symptoms and point to new therapeutic targets.

“We found that at peak infection time, there are distinct changes in different regions of the brain, including is a large decrease in mitochondrial genes in the cerebellum, the part of the brain that controls our muscles, balance, cognition, and emotion” said Schisler, assistant professor of pharmacology and member of the UNC McAllister Heart Institute. “The lung is the primary site of infection, but molecular signals are being transmitted affecting the entire body, with the heart, kidney, and liver being more affected than others, even long after the virus is gone.”

Treatments that may protect eggs against ageing

 

The spindle is responsible for separating the chromosomes equally when the oocyte goes through specialist meiotic cell divisions. The spindle is made of fibers called microtubules (green) to which the chromosomes (red) are attached. The use of MitoQ or BGP-15 improves the organization of the microtubules and alignment of the chromosomes to the center of the spindle. The oocyte has an improved chance of properly separating chromosomes and thereby avoiding aneuploidy when the egg is activated by the fertilizing sperm.

A woman’s fertility decreases as she ages – largely because of fewer healthy oocytes or eggs, and those that are available for fertilization often have chromosomal abnormalities which result in a higher incidence of miscarriage and genetic disorders such as Down’s syndrome.

Now a team at the Monash Biomedicine Discovery Institute (BDI) and Robinson Research Institute, collaborating with Monash IVF, has found a potential treatment that targets mitochondria to help prevent these chromosomal errors in mouse and human eggs.

In a paper published in the journal Human Reproduction, researchers led by Professors John Carroll and Rebecca Robker used two mitochondria-targeted therapeutics – called MitoQ and BGP-15 – which appeared to protect eggs from the chromosomal disturbances seen in older or abnormal eggs.

In particular, the addition of these agents improved how immature human eggs organize their chromosomes when matured in laboratory conditions. If this effect holds true for eggs maturing in the body it may also prevent chromosomal abnormalities in human eggs, effectively protecting them against miscarriage or genetic consequences such as Down’s syndrome.

The first author, Dr Usama Al-Zubaidi from the Monash BDI says: “Given that increasing numbers of women delay childbearing there is an imperative to improve fertility and reduce miscarriage and chromosomal anomalies associated with maternal ageing.”

The study identified “two excellent candidates that may one day help to improve fertility in older women.”

The age-related decline in fertility is strongly attributed to ovarian ageing, diminished ovarian reserves, and a decline in oocyte quality. One cause of this is due to increased oxidative stress within the oocytes.

Mitochondria – whether in an oocyte or any other cell in the body - use oxygen to create energy and one of the by-products is the production of free radicals. Oocytes are made during fetal life so have a lot of time to accumulate oxidative damage. Also, as eggs age, their defenses against oxidative damage become compromised. MitoQ and BGP-15 appear to be protecting eggs at least in part by improving mitochondrial function and minimizing oxidative stress during critical periods when the eggs are dividing their chromosomes.

Next steps involve finding the best conditions for these therapies to work when eggs are maturing inside the ovary and if the effects seen on chromosome organization translate into healthier eggs that have a better chance to develop into healthy pregnancies.

“Increasingly, fertility science is turning to therapies that specifically target these mitochondria with a view to preventing the chromosomal abnormalities that occur due to ageing and oxidative stress,” Professor Carroll said.

“Our study looked at two of these candidates to see whether they in fact made a difference to older eggs from humans and mice and found they can make the older eggs ‘younger’ again.” They were very effective at one level, but we are now working on seeing if this approach can work in patients.”

Both MitoQ and BGP-15 are used in humans already, – with MitoQ used to treat age associated hypertension while BGP-15 has been used in clinical trials for diabetes where it was given orally.

Medical Director Monash IVF, Professor Luk Rombauts said that improving function of the mitochondria, which he calls “the little energy factories within the eggs”, is one of the potential strategies to enhance egg quality and reproductive success, even more so in older women. “Monash IVF is keen to continue its collaboration with Professor John Carroll’s lab to find meaningful ways to turn this research into new treatment strategies.”

Source/Credit: Monash University

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New type of DNA damage found in our cells’ powerhouses

Linlin Zhao (left) and Yu Hsuan Chen
Photo Credit: Courtesy of University of California, Riverside

A previously unknown type of DNA damage in the mitochondria, the tiny power plants inside our cells, could shed light on how our bodies sense and respond to stress. The findings of the UC Riverside-led study are published in the Proceedings of the National Academy of Sciences and have potential implications for a range of mitochondrial dysfunction-associated diseases, including cancer and diabetes. 

Mitochondria have their own genetic material, known as mitochondrial DNA (mtDNA), which is essential for producing the energy that powers our bodies and sending signals within and outside cells. While it has long been known that mtDNA is prone to damage, scientists didn't fully understand the biological processes. The new research identifies a culprit: glutathionylated DNA (GSH-DNA) adducts.

An adduct is bulky chemical tag formed when a chemical, such as a carcinogen, attaches directly to DNA. If the damage isn’t repaired, it can lead to DNA mutations and increase the risk of disease.

How T cell assassins reload their weapons to kill and kill again

Cytotoxic T cells are specialist white blood cells that are trained by our immune system to recognize and eliminate threats – including tumor cells and cells infected with invading viruses, such as SARS-CoV-2, which causes COVID-19. They are also at the heart of new immunotherapies that promise to transform cancer treatment.

Professor Gillian Griffiths from the Cambridge Institute for Medical Research, who led the research, said: “T cells are trained assassins that are sent on their deadly missions by the immune system. There are billions of them in our blood, each engaged in a ferocious and unrelenting battle to keep us healthy.

“Once a T cell has found its target, it binds to it and releases its toxic cargo. But what is particularly remarkable is that they are then able to go on to kill and kill again. Only now, thanks to state-of-the-art technologies, have we been able to find out how they reload their weapons.”

Mitochondrial activation in transplanted cells promotes regenerative therapy for heart healing

Regenerative therapy to treat heart failure is more effective when the mitochondria of the regenerative cells are activated prior to treatment.
Image Credit: Gemini Advance

Heart failure stands as a leading cause of mortality worldwide, demanding advanced treatment options. Despite the urgency for more effective treatments, options for severe heart failure remain limited. Cell transplantation therapy has emerged as a promising ray of hope, as it can be used in regenerative therapy to heal the heart.

A research team led by Professor Yuma Yamada of Hokkaido University’s Faculty of Pharmaceutical Science has developed a technique to promote cardiac regeneration by delivering mitochondrial activators to cardiac progenitor cells. Their findings were published in the Journal of Controlled Release.

“Cardiomyocytes efficiently use the mitochondrial tricarboxylic acid cycle to produce large amounts of adenosine triphosphate from several substrates via oxidative phosphorylation (OXPHOS),” explains Yamada. “Based on the energy metabolism of cardiomyocytes, we hypothesized that activating the mitochondrial function of transplanted cells may improve the outcome of cell transplantation therapy.”

Molecular machines could treat fungal infections

Schematic representation of the mechanisms by which light-activated molecular machines kill fungi. Molecular machines bind to fungal mitochondria, decreasing adenosine triphosphate (ATP) production and impairing the function of energy-dependent transporters that control the movement of ions, such as calcium. This leads to the influx of water, which causes the organelles to swell and eventually the cells to burst.
Image Credit: Tour Group/Rice University

That stubborn athlete’s foot infection an estimated 70% of people get at some point in their life could become much easier to get rid of thanks to nanoscale drills activated by visible light.

Proven effective against antibiotic-resistant infectious bacteria and cancer cells, the molecular machines developed by Rice University chemist James Tour and collaborators are just as good at combating infectious fungi, according to a new study published in Advanced Science.

Based on the work of Nobel laureate Bernard Feringa, the Tour group’s molecular machines are nanoscale compounds whose paddlelike chain of atoms moves in a single direction when exposed to visible light. This causes a drilling motion that allows the machines to bore into the surface of cells, killing them.

Giant bacterium powers itself with unique processes

Micrograph of a group of Epulopiscium viviparus bacteria.
Image Credit: Esther Angert

Not all bacteria are created equal.

Most are single-celled and tiny, a few ten-thousandths of a centimeter long. But bacteria of the Epulopiscium family are large enough to be seen with the naked eye and 1 million times the volume of their better-known cousins, E. coli.

In a study published Dec. 18 in Proceedings of the National Academy of Sciences, researchers from Cornell and Lawrence Berkeley National Laboratory have for the first time described the full genome of one species of the family of giants, which they’ve named Epulopiscium viviparus.

“This incredible giant bacterium is unique and interesting in so many ways: its enormous size, its mode of reproduction, the methods by which it meets its metabolic needs and more,” said Esther Angert, professor of microbiology in the College of Agriculture and Life Sciences, and corresponding author of the study. “Revealing the genomic potential of this organism just kind of blew our minds.”

The first member of the Epulopiscium family was discovered in 1985. All members of the species live symbiotically within the intestinal tracts of certain surgeonfish in tropical marine coral reef environments, such as the Great Barrier Reef and in the Red Sea.