RIKEN researchers encapsulated actomyosin in cell-sized liposomes and found front-rear polarity emerging from mechanics alone, with no signalling network involved.
A migrating cell has to decide which end is the front. In living cells that decision is wrapped in a dense web of signalling — small GTPases, lipid gradients, feedback loops between them — and picking apart which parts are doing the deciding is difficult when all of it is present at once.
A study in Science Advances from RIKEN takes the other approach: build a cell with almost nothing in it and see what the remainder can do. Researchers constructed artificial cells from liposomes — membrane-bounded compartments the size of a real cell — encapsulating purified cytoskeletal proteins, and combined the experiments with computer simulations and theoretical analysis.
The work was done by the group of Makito Miyazaki at the RIKEN Center for Integrative Medical Sciences, with collaborators at Purdue University.
The finding is that the actin cytoskeleton can drive cell-scale shape changes and front-rear polarity on its own, without complex biochemical signalling.
What a bleb is
The specific shape change at issue is blebbing, and it is worth being precise about the mechanics because the whole result turns on them.
A cell’s membrane is not free-floating. It is tethered to a thin contractile meshwork just beneath it — the actomyosin cortex, actin filaments crosslinked and pulled on by myosin motors — and that cortex is under tension, which puts the cell’s interior under pressure. If the membrane detaches from the cortex at some point, or the cortex ruptures locally, pressure drives the bare membrane outward as a smooth spherical protrusion. That is a bleb.
It is not a curiosity. Blebbing is how some cells migrate, particularly through three-dimensional tissue where the flat crawling motion studied on glass does not work, and it is a recognised mode of invasion for cancer cells moving through confined spaces. Blebs also appear in cell division and in apoptosis.
When the artificial cells were physically manipulated in a particular way, they consistently developed a single membrane bleb — and single is the operative word. A compartment under uniform pressure with a uniformly weak cortex might be expected to bulge in many places or none; producing exactly one protrusion means something is concentrating the event at one location.
Breaking symmetry with nothing but mechanics
That concentration is the symmetry breaking in the paper’s title, and it is the reason the result is more than a demonstration of plumbing.
A liposome filled with actin and myosin is symmetric to begin with: no front, no back, no gradient of anything. For it to end up with one bleb and therefore one axis, the system has to select a direction spontaneously. The mechanism available is purely mechanical — once a bleb begins to form, it relieves pressure and draws in membrane, which makes a second bleb elsewhere less likely and the first one grow. A local event suppresses its own competitors.
“By reconstructing membrane morphogenesis from purified proteins, we showed that local interactions within the actin” network are sufficient, Miyazaki said, and the authors conclude that front-rear polarity can emerge from the mechanical properties of the actin cytoskeleton alone.
“By identifying the physical rules that govern cell shape, the present study lays important groundwork for numerous future” investigations, he said.
What reconstitution proves, and what it does not
Bottom-up reconstitution is a powerful method with one well-defined logical limit, and it is important not to overread the finding.
Building something from purified components demonstrates sufficiency: these ingredients, in this arrangement, can produce this behaviour. It does not demonstrate necessity, and it does not show that a real cell works this way. A living cell has the signalling network as well as the mechanics, and the fact that mechanics alone can break symmetry in a liposome leaves open how much of the work the signalling does in a cell that has both.
The most defensible reading is that the mechanical layer provides a floor. Signalling networks may bias, position and stabilise a polarity axis rather than create one from nothing — which is a different and more tractable problem than generating direction out of symmetry, and it is the kind of division of labour that is hard to establish any other way.
The liposome is also not a cell in several respects that bear directly on blebbing. Real cortices are linked to the membrane by specific proteins whose local detachment is what initiates a bleb in vivo, and real cells are attached to substrates and neighbours, which constrains where protrusions can form. An artificial cell lacks all of that, which is both the point of the experiment and a reason its mechanism need not be the one operating in tissue.
What the release leaves out
Two omissions are worth flagging.
The release describes the artificial cells as having been “physically manipulated” in a particular way without saying what the manipulation was — compression, shear, osmotic change, something else. Since the manipulation is what triggers the bleb, and therefore the thing a reader would want to know most, its absence makes the central experiment hard to assess from the release alone.
And there are no numbers at all: no liposome diameters, no protein concentrations, no bleb sizes or growth rates, no counts of how many compartments did this and how many did not. “Consistently developed a single bleb” is a frequency claim without a frequency.
The role of the simulations is also unclear from the release. The work combines experiment, simulation and theory, and which conclusions rest on which is the sort of thing that matters when a mechanism is being inferred — a physical rule confirmed by experiment and a physical rule reproduced in a model that was built to reproduce it are different kinds of evidence.
Why build a cell to study one
The applied framing in the release is broad — cell migration, cell division, embryonic development, drug discovery, regenerative medicine and synthetic biology all get a mention — and that breadth is a reason for scepticism about the specific promises rather than about the work.
The more contained case is methodological. Cell migration research has spent decades trying to attribute behaviours to particular molecules inside systems where everything is coupled to everything, and a preparation in which components can be added one at a time changes what can be asked. If cortical mechanics alone generate polarity, then the next experiment is to add one signalling component and see what it changes — which is an experiment that only becomes possible once the baseline exists.
The paper was published on 29 July 2026. The release names only Miyazaki, does not identify the Purdue collaborators or give a full author list, and states neither funding sources nor conflicts of interest.
Notes
- “Reconstitution of actomyosin networks in cell-sized liposomes dissects distinct mechanisms of membrane blebbing and symmetry breaking.” Science Advances, 2026. DOI: 10.1126/sciadv.aed8818. The release does not give the full author list.
- RIKEN. “A giant bleb for cell-kind: artificial cells reveal how living cells take shape.” EurekAlert!, 4 August 2026. https://www.eurekalert.org/news-releases/1138860.
Laura F. Bianchi/Centro de Regulación Genómica