By capping the tips of actin filaments, CD2AP reinforces the junctions between epithelial cells, Tang and Brieher show.
The actin cytoskeleton is a key structural element for intercellular junctions and dictates how tightly cells stick together. α-Actinin-4 is necessary for actin assembly at adherens junctions. However, the protein can’t do the job alone.
Tang and Brieher identified a protein complex at adherens junctions that contains 10 to 15 members and then tracked down proteins that reside near α-actinin-4 in the complex. One of those neighbors was CD2AP. The researchers found that CD2AP caps the barbed ends of actin filaments, preventing the attachment of actin monomers. The protein also prevented actin disassembly, Tang and Brieher showed.
To determine CD2AP’s effects on adhesion, the researchers devised a technique for measuring the strength of cell layers. They put single layers of epithelial cells above a chamber containing fluid. Pumping more fluid into the chamber put more pressure on the cells. Low pressures had no effect on the epithelial layer, even if CD2AP was scarce. But at high pressures layers lacking CD2AP ripped, indicating that the adherens junctions between cells had failed. The researchers conclude that CD2AP stabilizes actin filaments and helps the cells cling to each other.
Text by Mitch Leslie