MitoCatch delivers healthy mitochondria to diseased cells

Image Credit: Scientific Frontline

Scientific Frontline: Extended "At a Glance" Summary: MitoCatch

The Core Concept: MitoCatch is an advanced cellular delivery system designed to transplant healthy donor mitochondria directly into diseased or damaged cells. It acts as a targeted therapy to restore vital energy management in cells suffering from mitochondrial dysfunction.

Key Distinction/Mechanism: While traditional mitochondrial transplantation is inefficient and lacks precision in targeting, MitoCatch utilizes engineered docking proteins to act as cellular "match-makers." By precisely adjusting these proteins, the system guarantees that donor mitochondria bind exclusively to the correct target cell type and enter it, remaining fully functional to move, fuse, and divide.

Major Frameworks/Components: 

• MitoCatch-C: Equips target cells with docking proteins on their surface ex vivo so new mitochondria can attach and be absorbed before the cells are returned to the organism.
• MitoCatch-M: Modifies the donor mitochondria directly with docking proteins to guide them to unmodified target cells.
• MitoCatch-Bi: Utilizes a bispecific docking protein that acts as a bridge, connecting completely unaltered donor mitochondria to unaltered target cells.

High-intensity interval training boosts muscle power plants

Photo Credit: Sven Mieke

Scientific Frontline: Extended "At a Glance" Summary: High-Intensity Interval Training and Mitochondrial Adaptation

The Core Concept: High-intensity interval training (HIIT) enhances muscle energy production not just by increasing the total number of mitochondria, but by physically expanding the density of their active inner membranes, known as cristae.

Key Distinction/Mechanism: While previous research established that exercise generates more cellular power plants (mitochondria), this study proves that exercise also fundamentally upgrades their internal structure. By packing more cristae folds into the same space, existing mitochondria become vastly more efficient at producing energy (ATP) without requiring the overall mitochondrial network to expand. Furthermore, this structural adaptation occurs equally in healthy individuals, those who are overweight, and those with type 2 diabetes, disproving the common assumption that diabetes inherently impairs muscular adaptation to exercise.

Major Frameworks/Components: 

• Mitochondria: The cellular structures responsible for converting energy from food into the specific type of energy utilized by muscles.
• Cristae Density: The folded inner membranes of mitochondria where active energy production occurs; an increase in density provides a larger working surface area for energy output.
• Muscular Plasticity: The physiological capacity of muscle tissues to alter their microscopic structure and metabolic efficiency in response to high-intensity physical stress.
• ATP (Adenosine Triphosphate) Synthesis: The biochemical process of generating cellular energy, directly boosted by the expansion of the mitochondrial active membrane.

Mitochondria as Control Centers of Cell Communication

Anna Meichsner is investigating the role of mitochondria.
Photo Credit: © RUB, Marquard

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Mitochondria operate as central signaling hubs that actively control cellular communication by linking metabolic states with stress and immune responses, moving beyond their traditional role as energy producers.
• Methodology: Researchers from Ruhr University Bochum analyzed and systematized the functional roles of mitochondria in intracellular signaling and innate immunity, publishing a comprehensive review in Molecular Cell.
• Key Data: Mitochondria release specific signaling molecules including reactive oxygen species, metabolites, and nucleic acids which possess bacterial-like signatures that the cell identifies as danger signals to trigger immune activation.
• Significance: The identification of mitochondria as critical interfaces for cellular stress and immune responses explains the mechanism connecting mitochondrial dysfunction to the development of metabolic, neurodegenerative, and inflammatory diseases.
• Future Application: Clarifying these regulatory mechanisms enables the development of targeted medical interventions that modulate pathological signaling processes to treat chronic inflammation and associated disorders.
• Branch of Science: Biochemistry and Cell Biology
• Additional Detail: The study reveals a dual nature of mitochondrial signaling, where controlled release enhances immunity but unregulated release provokes chronic inflammation, marking a pivotal shift in understanding disease pathology.

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.

Paternal mitochondria turn out to be less rare than thought

Tobacco Plant
Photo Credit: Michael Schreiber 

Scientific Frontline: Extended "At a Glance" Summary: Paternal Mitochondrial Inheritance in Plants

The Core Concept: Paternal mitochondrial inheritance is the transmission of mitochondrial DNA from a male parent to its offspring, a biological phenomenon recently proven to occur in plants far more frequently than the traditional paradigm of strict maternal inheritance dictates.

Key Distinction/Mechanism: While standard genetic models state that cytoplasmic genomes (such as those in mitochondria and chloroplasts) are exclusively passed down through the maternal egg cell, "paternal leakage" allows male organelles to survive and be inherited. This transmission rate is governed by specific exonuclease enzymes that normally degrade cytoplasmic DNA in pollen; inhibiting these enzymes, along with applying environmental stressors like cold temperatures, bypasses the maternal-only safeguard and exponentially increases paternal mitochondrial transmission.

Origin/History: This research was spearheaded by plant biologist Kin Pan Chung and an international collaborative team from Wageningen University & Research (WUR), the Max Planck Institute of Molecular Plant Physiology (MPIMP), and The Chinese University of Hong Kong (CUHK).

Major Frameworks/Components: 

• Cytoplasmic Genomes: The distinct DNA housed within extranuclear cellular organelles—specifically mitochondria (the cell's energy factories)—which operate independently of the primary DNA package in the cell nucleus.
• Paternal Leakage Quantification: Previous assumptions held that paternal transmission of mitochondria did not occur in most flowering plants. Researchers established a natural leakage baseline of 0.18% in tobacco plants, a significant deviation from the accepted rule.
• Exonuclease Activity: Specific exonuclease enzymes act as biological gatekeepers by actively cutting up and degrading mitochondrial DNA within pollen.
• Environmental Modulation: Cold treatment applied to paternal plants induces a higher concentration of organelles in sperm cells. When combined with an exonuclease mutation, the paternal inheritance rate can be artificially raised to over 7%.

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.

CRISPR-based technique unlocks healing power of mitochondria for heart failure therapy

Mario Escobar
Photo Credit: Jeff Fitlow/Rice University

Scientific Frontline: "At a Glance" Summary: CRISPR-Based Mitochondrial Therapy for Heart Failure

• Main Discovery: Researchers at Rice University and Baylor College of Medicine utilized a nonediting CRISPR technique to safely increase mitochondrial production in heart cells, improving cellular energy levels without causing cellular burnout or malfunction.
• Methodology: The scientific team developed a nonediting CRISPR system that functions as an activation switch. Instead of editing the genome or forcing gene overproduction, the system fine-tunes natural regulatory pathways, specifically targeting the PPARGC1A gene, to prompt human cardiomyocytes to assemble more mitochondria in a measured way.
• Key Data: Heart failure is fundamentally a cellular energy crisis that currently impacts 6.8 million Americans, carrying a high lifetime risk where 1 in 4 adults in the United States are expected to develop the condition.
• Significance: The system successfully improved the rate of oxygen consumption and overall mitochondrial function across various models, including animal models and adult human heart donor tissue from both normal and diseased hearts, addressing the root cause of cardiac energy deficiency.
• Future Application: This approach offers a promising foundation for developing sustainable treatments for heart failure and other metabolic diseases by actively restoring impaired cellular energy supply rather than conventional approaches that merely reduce cardiac energy demand.
• Branch of Science: Molecular Biology, Bioengineering, Cardiology, and Genetics

MIC13 and Mitochondrial Liver Disease

The graphic shows how damage to the cristae affects cell metabolism and the extracellular environment, and can thereby contribute to the development of mitochondrial liver disease.
Image Credit: © HU/Ruchika Anand/AI-generated 

Scientific Frontline: Extended "At a Glance" Summary: MIC13-Linked Mitochondrial Liver Disease

The Core Concept: Mitochondriopathies are severe cellular disorders caused by damaged mitochondria, the energy-producing centers of the cell. A specific variant of the MIC13 protein disrupts the mitochondria's internal structure, driving early-stage liver disease.

Key Distinction/Mechanism: Unlike the previous assumption that cellular environmental changes are merely a consequence of advanced liver damage, a disease-causing MIC13 variant directly disrupts the inner mitochondrial membrane folds (cristae). This structural failure immediately alters amino-acid, lipid, and energy metabolism, which in turn triggers increased collagen accumulation and early fibrotic remodeling in the extracellular matrix.

Major Frameworks/Components:

• Mitochondrial Cristae Architecture: The structural folds of the inner mitochondrial membrane, organized by the MIC13 protein, which are critical for proper cellular metabolic function.
• Extracellular Matrix (ECM) Remodeling: The structural support network surrounding cells that undergoes early fibrotic changes, such as abnormal collagen accumulation, due to mitochondrial dysfunction.
• Pluripotent Stem Cell Modeling: Advanced cell models genetically modified to generate liver cells that accurately display key features of mitochondrial disease, bypassing previous research limitations.

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

Sub-Zero Microscopy Explores Antarctic Fish Cells

Harpagifer fin mitochondria and nucleic acid.
Photo Credit: Francesca van Tartwijk, Anne-Pia Marty, and Amir Rahmani

Scientific Frontline: Extended "At a Glance" Summary: Sub-Zero Live-Cell Microscopy and Antarctic Fish Adaptation

The Core Concept: Researchers engineered a novel microscope capable of operating near 0 degrees Celsius, enabling the first-ever high-resolution observations of living Antarctic fish cells to understand their survival mechanisms in extreme cold.

Key Distinction/Mechanism: Unlike the slow whole-body development of cold-adapted organisms, their intracellular movement remains remarkably fast. To combat the inefficiency of protein synthesis and the high rate of protein misfolding caused by cold, cells of the Antarctic spiny plunderfish (Harpagifer antarcticus) feature enlarged lysosomes for waste disposal and fused, networked mitochondria for enhanced energy production.

Origin/History: On September 23, 2026, a research team led by the British Antarctic Survey and the University of Cambridge's Department of Chemical Engineering and Biotechnology announced this technological microscopy breakthrough alongside the first successful culturing of Antarctic fish cells.

Major Frameworks/Components:

• Sub-Zero Fluorescence Microscopy: Custom-engineered imaging technology that captures high-resolution, dynamic images of living cells at temperatures near freezing without damaging the extremophile specimens.
• Extremophile Cell Culturing: Novel laboratory techniques developed to isolate and maintain live cells from Harpagifer antarcticus for comparative cellular analysis against temperate species, such as the shanny (Lipophrys pholis).
• Mitochondrial Networking: A cellular adaptation in which mitochondria merge into larger, interconnected networks to optimize energy production and protect themselves in cold environments.
• Lysosomal Degradation: The utilization of enlarged lysosomes acting as cellular recycling centers to efficiently break down and dispose of harmful, misfolded proteins.

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.

PINK1 Gene Protects Neurons in Parkinson's

Image Credit: Scientific Frontline / stock image

Scientific Frontline: Extended "At a Glance" Summary: Mitochondrial DNA Damage and the PINK1 Gene in Parkinson's Disease

The Core Concept: A protective genetic response, driven by the PINK1 gene, attempts to preserve energy production in vulnerable brainstem neurons by mitigating extensive mitochondrial DNA damage in patients with Parkinson's disease.

Key Distinction/Mechanism: Rather than focusing on dopamine-producing cells, this mechanism targets acetylcholine-producing neurons. The PINK1 gene initiates a quality-control process that identifies damaged mitochondria and targets them for removal, preserving cellular energy and overall function.

Origin/History: Published in the journal "Brain" on October 7, 2026, this research by Newcastle University and the University of Birmingham represents the first single-cell analysis of mitochondrial DNA in this specific neuronal population.

Major Frameworks/Components:

• Single-cell mitochondrial DNA sequencing and computational analysis of post-mortem brain tissue.
• Identification of large-scale deletions within the "major arc" region of mitochondrial DNA, which is critical for generating cellular energy.
• Increased expression of the PINK1 mitochondrial quality-control gene as a cellular defense mechanism.
• Analysis of acetylcholine-producing brainstem neurons linked to sleep, cognition, gait, and balance.

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.