If it walks like a duck and quacks like a duck, it must be a duck….or it could be me doing my best duck impression. Scientists don’t like to make assumptions, but instead are driven to painstakingly test the cellular unknowns. Today’s image is from a paper that serves as a good example of how assumptions may not be accurate, but instead lead to a fascinating story that prompts more questions.
Desmosomes are cell-cell adhesion structures that help tissues resist mechanical stress by connecting with the cells’ intermediate filament networks. The mechanical strength provided by desmosomes is well documented in tissues such as heart muscle and stratified epithelia (skin, esophagus, etc). The intestine is a simple epithelial tissue that contains desmosomes, and as it is under a lot of mechanical stress from the movement and content of digesting food, it can be easily assumed that the desmosomes in intestinal tissue provide mechanical support. Not so, according to a recent paper by Sumigray and Lechler. The desmosomal protein desmoplakin (DP) is not essential for cell adhesion or tissue integrity in intestinal epithelia, nor is it necessary for proper organization of keratin intermediate filaments. However, DP is important for the structure of microvilli, the actin-rich structures that provide surface area for the absorption of nutrients. As seen in the images above, the microvilli of intestinal cells from DP knockout mice (middle, right) are shorter and misshapen when compared to wild-type cells (left).
Sumigray, K., & Lechler, T. (2012). Desmoplakin controls microvilli length but not cell adhesion or keratin organization in the intestinal epithelium Molecular Biology of the Cell, 23 (5), 792-799 DOI: 10.1091/mbc.E11-11-0923