Forget about lotions and facial creams. The secret to good—or at least strong—skin is β-catenin, Ray et al. reveal.

β-Catenin bolsters the adherens junctions that fasten epithelial cells together. But previous work suggested that the protein wasn’t important in the skin. Mice lacking β-catenin in the epidermis have normal skin if β-catenin is eliminated after birth, although the protein’s function during embryonic development remains uncertain.

Ray et al. deleted the protein from the epidermis of developing mouse embryos. These animals died shortly after birth because their skin was porous. The researchers found that, in their paw skin, embryos lacking β-catenin lost many of the tight junctions that interlock cells and make the skin watertight. The skin on an embryo’s paws is likely to be under mechanical stress because the paws are still growing and start moving before birth. The flaws in the knockout animals suggest that β-catenin strengthens the skin against mechanical stress.

The researchers tested this idea in cultured skin cells. Pulling on cells that lack β-catenin spurred their tight junctions to break down. Cells under tension typically bolster their adherens junctions with vinculin, which connects the junction to the actin cytoskeleton. But Ray et al. discovered that cells lacking β-catenin didn’t direct vinculin to their adherens junctions. This suggests that β-catenin helps fortify adherens junctions under mechanical stress, which, in turn, leads to the strengthening of tight junctions. How changes to the adherens junctions alter the tight junctions is a question for future research.

et al
J. Cell Biol.

Author notes

Text by Mitch Leslie