The intestinal epithelium is characterised by rapid cell turnover, with pluripotential stem cells in the crypts of Lieberkühn providing a continuous supply of cells which are directed into a variety of maturation pathways. Development and maintenance of normal intestinal epithelial morphology requires regulation of daughter cells’ proliferative status, lineage allocation, migration, differentiation, and apoptosis.1 It has become increasingly evident that co-ordination of these processes and the consequent generation of the characteristic intestinal epithelial architecture are highly dependent on intercellular and cell-matrix adhesive interactions.2These adhesive events are not random, but through selective interactions, organise cells into diverse and highly distinctive patterns. Connections of cell junctions such as desmosomes, hemidesomosomes, and adherens junctions to the actin cytoskeleton, thus allow maintenance of cell polarity and tissue architecture.3 Variation in the functional state of these adhesive mechanisms is critical to the dynamic processes necessary for tissue morphogenesis in the embryo,4 where many morphogenetic events are correlated with a unique spatiotemporal pattern of cadherin expression.5 Such variation is also critical to the maintenance of this highly complex architecture in various physiological and pathological states, such as migration of cells up the crypt-villus axis6 and repair of mucosal injuries. In view of these facts, it is not surprising that many cell adhesion molecules have been implicated in cell signalling pathways.7 ,8