Rather, they are collectives of interacting cells that give rise to tissues and organs. Our department seeks to answer these questions at several levels by attempting to link genetic regulation to the mechanochemical processes that coordinate cell division, cell movement, and cell death. CAMs are involved in defining cell collectives and the borders of these groups of cells as the collectives interact during inductive events in morphogenesis. Networks of SAMs are involved in patterned cell migration. Although CAMs cannot be considered the cause of induction, they play major constraining roles in complex chains of inductive interactions that involve hormones and growth factors, components of the extracellular matrix, and cellular receptors.
CAMs function in neurite guidance and fasciculation, cell migration, and regeneration.
Each CAM studied so far is specified by a single gene, although the genomic structures of different CAMs vary widely. Perturbation of CAM binding can lead to changes in morphology. During morphogenesis and regeneration, CAMs are coregulated with SAMs to affect migration and positioning. An example is tenascin, an extracellular matrix protein that supports counteradhesive events. This molecule may be one of a series of molecules controlled by neural signals that affect migration of cells and neurites into particular sites.