The study, led by Philipp Radler in the laboratory of Christa Schleper at the University of Vienna and published in the journal Nature, provides the first direct observations of Asgard archaeal motility. These organisms are tiny; each cell has a volume roughly a thousand times smaller than that of a human cell. Yet the recordings show them undergoing dramatic transformations of shape on a minute-by-minute basis, extending thin appendages that can reach up to twenty times the length of the cell body, retracting them again, and using them to actively explore their surroundings. The behavior is strikingly reminiscent of the amoeboid movement seen in far more sophisticated cells, including human immune cells patrolling tissue.

Why does this matter so much? Asgard archaea occupy a central position in current models of eukaryogenesis, the process by which the first complex cells emerged roughly two billion years ago. The prevailing scientific framework holds that a eukaryotic ancestor arose from a symbiotic fusion between a bacterium and an archaeal lineage ancestral to today’s Asgard archaea. In that scenario, the bacterium eventually became the mitochondrion, the energy-producing organelle that powers virtually every complex cell on Earth. Asgard archaea are therefore not merely an interesting branch of the microbial tree; they are the closest available window into the cellular world from which our own lineage was born.

Until very recently, that window was almost entirely opaque. The first Asgard archaea were only brought into culture in 2020 and 2023, one at the JAMSTEC Institute in Japan and another in Schleper’s laboratory in Vienna, and both Japanese teams are co-authors on the new study. Before those milestones, essentially everything scientists knew about the group came from DNA sequencing of environmental samples or from electron microscopy of fixed cells. Those static images were already tantalizing: they showed a round cell body surrounded by a halo of fine, branching projections. But a fixed image cannot reveal whether a cell is extending, retracting, or moving, and so the functional significance of these elaborate shapes remained a matter of speculation.

The Vienna team closed that gap with a technically demanding approach. Asgard archaea are anaerobes, organisms that cannot tolerate oxygen, so the researchers placed the cells in an oxygen-free environment and filmed them alive under the microscope. They worked with two strains: a Lokiarchaeon cultivated in Vienna and a Heimdallarchaeon cultivated in Japan. Both organisms displayed the same remarkable repertoire of behaviors, drastically reshaping themselves every minute and deploying their thin, dynamic appendages to attach to surfaces and probe them. The crawling motion they use had not previously been described in any microbe, and its closest parallels lie in the motility of complex eukaryotic cells.

The mechanistic story behind the movement is equally significant. When the team applied actin inhibitors to the cultures, the dynamic behaviors were suppressed. Actin is one of the fundamental components of the cytoskeleton, the internal scaffolding that gives cells their shape, drives their internal transport, and powers their movement. In eukaryotes, an actin-based cytoskeleton underlies everything from muscle contraction to the crawling of immune cells through tissue. Finding that the motility of Asgard archaea likewise depends on actin suggests that a functional actin cytoskeleton, with clear parallels to the one operating in human cells, was already in place in the archaeal lineage long before the first eukaryote existed.

The international collaboration behind the study included, alongside the Japanese microbiologists, researchers from the Institute of Science and Technology Austria and the Helmholtz Centre for Infection Research in Braunschweig, Germany. Their combined expertise in cultivation, microscopy and cell biology was essential to a result that no single laboratory could have achieved alone. Culturing Asgard archaea remains extraordinarily difficult; the organisms grow slowly, in strict anaerobic conditions, and only a handful of laboratories worldwide have managed it. Every live-cell observation therefore represents years of methodological groundwork.

From an evolutionary standpoint, the discovery opens a genuinely new perspective on the deep history of cellular innovation. Complex cell motility may have far older origins than previously assumed, predating the emergence of eukaryotes themselves. If the ancestor of Asgard archaea already possessed the machinery for shape change, surface attachment and crawling, then some of the cellular capabilities once thought to be eukaryotic inventions may instead have been inherited from their archaeal partner. Such capabilities could even have played a role in the ancient symbiosis from which mitochondria later emerged, potentially facilitating the physical interactions between the archaeal host and its bacterial partner that set complex life in motion.

The findings also carry practical implications that extend well beyond evolutionary theory. Because the actin cytoskeleton governs shape changes and motility in human cells, understanding a simpler, archaeal version of the same machinery offers a comparative framework for dissecting how this fundamental system works. Insights gained from organisms that sit at the evolutionary boundary between prokaryotes and eukaryotes can illuminate which features of the eukaryotic cytoskeleton are ancient inheritances and which are later refinements. In this sense, the humble Asgard archaea, invisible to the naked eye and difficult to culture, may help explain processes that are central to human biology, including immune cell migration and cellular architecture.

Perhaps the most consequential aspect of the study is methodological. Oxygen-free live-cell microscopy of Asgard archaea now makes it possible, for the first time, to test models of the origin of complex life against empirical observation rather than inference from genomes and static images. Hypotheses about how the first eukaryotes moved, attached to surfaces, and interacted with partner cells can now be confronted with real footage of their closest living relatives in action. What has emerged from those first recordings, dynamic protrusions, actin-dependent crawling and a fluidity of form once thought to belong exclusively to complex cells, suggests that the road to eukaryotic life may have been paved with cellular behaviors far older and far more sophisticated than anyone had imagined.

Subject of Research: Crawling motility and actin-based cytoskeleton dynamics in Asgard archaea and their implications for eukaryogenesis

Article Title: Unexpected dynamics of ancient microbes discovered

Article References: Unexpected dynamics of ancient microbes discovered. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: Asgard archaea, Lokiarchaeon, Heimdallarchaeon, eukaryogenesis, actin cytoskeleton, cell motility, crawling motility, live-cell microscopy, mitochondria, evolution, University of Vienna, Nature

Macroautophagy, the best-studied form of autophagy, is an intracellular degradation system that is essential for cellular homeostasis. In this process, a double-membraned vesicle called an autophagosome forms around cytoplasmic cargo, including damaged organelles and aggregated proteins, and delivers the cargo to the lysosome or vacuole for destruction and recycling. Building an autophagosome requires the concerted action of around twenty autophagy-related genes, known as ATG genes, together with components of the cytoskeleton and the endomembrane systems. Because this machinery involves membrane deformation on a massive scale, its origin poses a striking evolutionary puzzle: how did a process requiring such elaborate coordination arise in the first eukaryotic cells?

The review argues that the autophagy pathway likely already existed in the last eukaryotic common ancestor, often abbreviated LECA, the hypothetical organism from which all living eukaryotes descend. This conclusion rests on the observation that core components of the autophagy machinery are found across the major eukaryotic supergroups, suggesting that the pathway was present before those groups diverged. Rather than being an invention of any single lineage, autophagy appears to be an ancestral eukaryotic innovation that was subsequently modified, expanded or trimmed as different branches of the eukaryotic tree pursued their own evolutionary paths.

Interestingly, the pathway itself does not exist in prokaryotes. Bacteria and archaea lack autophagosomes, lysosomes and the endomembrane systems on which eukaryotic autophagy depends. Yet when researchers search prokaryotic genomes for sequences resembling ATG genes, they find remote homologs of several of them. These distant relatives of eukaryotic autophagy genes hint that the raw materials from which the autophagy machinery was built were available long before eukaryotic cells existed, and that the pathway was assembled by repurposing pre-existing protein modules for new cellular functions.

Zhang and Mizushima organize their review around three major themes. The first concerns the evolutionary context surrounding the emergence of the autophagy pathway during eukaryogenesis, the series of events by which complex eukaryotic cells arose from prokaryotic ancestors. The second addresses how ATG genes diversified in different eukaryotic lineages through gene duplications, gene losses, and lineage-specific gains, producing the varied complements of autophagy genes observed in fungi, plants, animals and protists today. The third explores the functions that remote homologs of ATG genes carried out in prokaryotes and the phylogenetic and evolutionary relationships linking the eukaryotic and prokaryotic versions of these genes.

The eukaryogenesis story is central to understanding autophagy’s origin. The autophagosome depends on membranes, vesicle trafficking and cytoskeletal dynamics, all hallmarks of the eukaryotic cell plan. As the ancestors of eukaryotes acquired endomembrane compartments and an elaborate cytoskeleton, the molecular tools needed for autophagosome formation became available. The review suggests that the pathway’s emergence was tied to this broader cellular transformation, with ancestral protein families that carried out simpler membrane-related or stress-related functions in prokaryotes being recruited and elaborated into the coordinated autophagy machinery of early eukaryotes. In this view, autophagy is not an isolated invention but an integrated product of the cellular revolution that created the eukaryotic cell.

The diversification of ATG genes across eukaryotic lineages reveals how evolution both conserves and reshapes essential systems. Core autophagy genes have been retained across vast evolutionary distances, reflecting the fundamental importance of intracellular degradation to cell survival. At the same time, gene duplications have produced expanded families in some lineages, allowing functional specialization of related proteins, while gene losses have streamlined the machinery in others, and lineage-specific gains have introduced novel components not found elsewhere. These patterns mean that different organisms deploy partially distinct sets of ATG proteins to accomplish a fundamentally conserved process, and they complicate the task of identifying autophagy genes by sequence similarity alone, particularly in poorly studied protist groups.

The prokaryotic homologs of ATG genes add an intriguing dimension to this picture. Although bacteria and archaea do not perform macroautophagy, several of their proteins are recognizably related in structure or sequence to eukaryotic autophagy factors. Understanding what these remote homologs do in prokaryotic cells, whether they handle membrane remodeling, stress responses, protein trafficking or other tasks, offers clues about the ancestral functions from which autophagy components were drawn. Tracing the phylogenetic relationships between the eukaryotic and prokaryotic versions of these genes helps distinguish scenarios in which eukaryotes inherited the genes vertically from archaeal ancestors from those in which lateral gene transfer or other routes contributed to the modern complement of autophagy factors.

The implications of this evolutionary perspective extend well beyond comparative genomics. Autophagy is implicated in human health in contexts ranging from neurodegenerative disease to cancer and immunity, and much of what is known about the pathway comes from studies of yeast and mammalian cells. Recognizing which components are ancestral and universal, which are lineage-specific innovations, and which features of the machinery have been reshaped by evolution can guide researchers in choosing appropriate model systems and in interpreting similarities and differences between organisms. The review’s evolutionary framework provides a map for predicting where the pathway may vary and which of its elements represent the ancient core.

Zhang and Mizushima also look forward, outlining possible future directions for the field. These include filling in the distribution of autophagy genes across under-sampled eukaryotic lineages to better resolve when and how duplications and losses occurred, deepening the functional characterization of prokaryotic homologs to illuminate the pre-eukaryotic roles of ancestral proteins, and refining models of eukaryogenesis to place autophagy’s emergence within a firmer chronology. As genome data from diverse organisms continue to accumulate, the authors anticipate that the boundary between what is known about autophagy in model organisms and what can be inferred across the tree of life will continue to blur, yielding a more complete account of how one of the cell’s most sophisticated degradation systems came to be.

The review, which is open access, was supported by a Grant-in-Aid for Specially Promoted Research from the Japan Society for the Promotion of Science awarded to Noboru Mizushima. By gathering the threads of genomics, phylogenetics and cell biology into a single evolutionary narrative, the work underscores a theme that resonates throughout modern biology: even the most intricate molecular machines of complex cells are built from parts with far older histories, and reconstructing those histories is essential for understanding how the machinery works today.

Subject of Research: Evolutionary origins and diversification of autophagy-related genes across prokaryotes and eukaryotes

Article Title: Autophagy genes across the tree of life: from prokaryotic homologs to eukaryotic complexity

Article References: Zhang, S., & Mizushima, N. (2026). Autophagy genes across the tree of life: from prokaryotic homologs to eukaryotic complexity. Cellular and Molecular Life Sciences. https://doi.org/10.1007/s00018-026-06423-7

Image Credits: AI Generated

DOI: 10.1007/s00018-026-06423-7

Keywords: autophagy, ATG genes, macroautophagy, eukaryogenesis, last eukaryotic common ancestor, prokaryotic homologs, gene duplication, genome evolution, phylogenetics, autophagosomes, cellular degradation, evolution