A protein that stabilizes microtubules also helps maintain desmosomes, Sumigray et al. report.
Desmosomes fasten cells together in organs such as the heart and skin that have to withstand intense mechanical stress. Defects in these structures cause problems such as skin blistering and cardiomyopathy. But desmosomes are more than just cellular Velcro. As some cells differentiate, microtubules no longer radiate out from the centrosome and instead localize to the cell cortex. The researchers have previously found that, during this processs in epithelial cells, the desmosome protein desmoplakin lures another protein, ninein, from the centrosome to the desmosome.
The researchers discovered that two other centrosome proteins, Lis1 and Ndel1, also make the jump to desmosomes and that desmoplakin recruits both of them. Lis1 and Ndel1 help organize microtubules in other contexts, making them good candidates for reconnecting microtubules to the cortex. To test that possibility, the researchers created mice that are missing Lis1 in their epidermis. In the animals’ epidermal cells, the microtubules did not reorganize, indicating that Lis1 is necessary for this rearrangement. Sumigray et al. also discovered that Lis1 may have an additional desmosomal function. The Lis1-lacking animals died as newborns because their skin was permeable. Desmosomes were faulty in these animals, suggesting that Lis1 helps stabilize the structures. The next question is how Lis1 performs that function.
