According to the study, researchers explaining the anatomical feature of the cells pack in the epithelial tissues; as the cells in an epithelial sheet are normally connecting by the Velcro-like structures called adhesive junctions and have a near-uniform size distribution. As a result, cells related by descent tend to stick together in mosaic patches referred to as cell clones. In the fruit fly Drosophila melanogaster; epithelial cell clones that have smaller cells can lose contact with each other and disperse among their neighbors.
As epithelia are cell sheets that act as a barrier to protect the body from the external environment. The epithelial barrier is critical to maintain body homeostasis, and its disruption has been linked to various diseases; including atopic dermatitis and inflammatory bowel diseases. In order to maintain the epithelial barrier; it is important to completely seal the space between cells to restrict the movement of substances across the epithelial sheet, and that is the task that tight junctions fulfill.
The epithelial tissues
According to the study this explaining that small-cell clones in proliferating epithelia tissues; that line all body surfaces organize very differently than their normal-sized counterparts. A common feature of many cancer types is the pleomorphic nature or variability in size and shape of cells in a tumor. In examining these cells, the researchers find that claudins form a barrier against small molecules including ions. To their surprise, loss of claudins did not lead to separation of the two neighboring cells.
One of the most astounding feats of developmental biology is the transformation of an epithelial sheet into a functionally specializing three-dimensional structure. To do so, epithelial systems rely on uniformity among cells. Developmental processes shape and sculpt epithelia by creating region-specific properties; that are classically understanding to be driving by molecular pathways. In the human body, which is primarily made up of epithelial cell layers; the vast majority of mutations we accumulate are not germline, but rather somatic, and therefore clonal in nature.
Clones of cells
In a pathogenesis context, because mutations create clonal effects; we don’t have a framework for thinking about how clones of cells behave when they’re genetically distinct from the surrounding wild type cells; but it’s extremely important. The Gibson Lab continues to build off this study and related work to understand the interaction between physically and genetically heterogeneous epithelial cell populations.
The study showing that epithelial barrier is making by a combination of two distinct systems; a tight barrier against small molecules made by claudins, and a crude barrier against large molecules made by JAM-A. However, when we noticing that JAM-A was more accumulating at cell junctions lacking claudins; we started to think that JAM-A may be maintaining the barrier against large molecules