Creating artificial cells with realistic characteristics from a minimal set of components is a major goal of synthetic biology. Autonomous movement is a key ability here, difficult to replicate in the test tube. A team led by physicist Erwin Frey, professor of statistical and biological physics at LMU, and Petra Schwille of the Max Planck Institute for Biochemistry, has now made a significant breakthrough in this area, as the researchers report in the journal Natural Physics.

The scientists succeeded in keeping vesicles surrounded by a lipid membrane – called liposomes – in constant motion on a support membrane. This movement is driven by the interaction of the vesicle membrane with certain protein patterns, which in turn require the biochemical “fuel” ATP. These models are generated by a system known for the formation of biological models: the Min protein system, which controls cell division in the E. coli bacterium. Experiments in Schwille’s lab showed that the artificial system’s membrane-binding Min proteins organize asymmetrically around the vesicles and interact with them in ways that set them in motion. In the process, the proteins bind both to the supporting membrane and to the vesicles themselves. “Directed transport of large membrane vesicles is otherwise only found in higher cells, where complex motor proteins accomplish this task. Finding out that small bacterial proteins are capable of something similar was a total surprise,” observes Schwille. “It is currently unclear not only what exactly protein molecules do on the surface of the membrane, but also for what purpose bacteria might need such a function.”

Two possible mechanisms

Using theoretical analyses, Frey’s team identified two different mechanisms that might be driving the movement: “One possible mechanism is that proteins on the support membrane interact with those on the surface of the vesicle kind of like a zipper and form or dissolve molecular compounds in that way,” says Frey. “If there is more protein on one side than the other, the zipper opens there, while it closes on the other side. The vesicle therefore moves in the direction where there is less protein.” The second possible mechanism is that membrane-bound proteins deform the vesicle membrane and alter its curvature. This change of shape then causes the forward movement.

“Both mechanisms are possible in principle,” Frey points out. “What we do know for certain, however, is that the protein patterns on the supporting membrane and on the vesicle cause the movement. This represents a big step forward on the way to artificial cells.” The authors are confident that their system can serve as a modeling platform in the future for the development of artificial systems with realistic movements.