KARLSRUHE, Germany – Cell membrane repair in a living organism was observed in real time using a high-resolution fluorescence imaging technique. The findings may contribute to the development of therapies for human myopathies and pave the way for new biotechnology methods.
Every cell in the body is enclosed by a thin double layer of lipids, called a plasma membrane, which separates the distinct internal environment of the cell from the extracellular space. Damage to this bilayer disturbs cellular functions and could result in the death of the cell. To prevent irreparable damage, muscle cells have efficient systems that seal the little holes in the plasma membranes; e.g., tears made in the membrane of leg muscles as you walk downhill.
Now, researchers at Karlsruhe Institute of Technology (KIT) and Heidelberg University have observed the cell membrane repair of a zebra fish in real time.
Repair of the plasma membrane of a cell: For the first time, researchers have observed the relevant repair mechanisms in zebra fish. Courtesy of Institute of Toxicology and Genetics, KIT.
The scientists tagged repair proteins with fluorescent proteins in the muscle of transparent zebra fish larvae. Then, with a laser, they burned tiny holes into the plasma membrane of its muscle cells and observed the repair of the holes under a microscope. Their experiment showed that membrane vesicles – together with proteins dysferlin and annexin A6 – rapidly form a repair patch. Other annexins accumulate subsequently on the injured membrane.
The studies suggest that the cell assembles a multilayered repair patch from the inside that seals off the cell’s interior from the extracellular environment. The scientists also discovered that there is a specialized area that quickly supplies the material needed for sealing the plasma membrane hole.
This animal model for membrane repair will contribute to the identification of new proteins in the sealing process and will clarify the underlying mechanisms.
The work was published in Developmental Cell
(doi: 10.1016/j.devcell.2011. 12.008