Cell–matrix interactions are important in the development of the avian cornea. Type VI collagen is present within the periocular mesenchyme prior to the migration of cells into the corneal stroma and is abundant in the mature stroma. Whether the interaction of cells with type VI collagen is essential for cellular survival in the cornea is not known. In the present study, we examined the interaction of corneal cells with type VI collagenin vitroto determine if it can increase cell proliferation and decrease apoptosis.In vivoanalysis demonstrated that apoptosis occurs in the periocular region during early stages of avian corneal development, but in fully mature corneas apoptosis only occurs in the corneal epithelium and not in the stroma.In vitroanalysis examined the importance of β₁integrin interactions with type VI collagen in mature corneal fibroblasts and the precursor cells. Using an anti-β₁integrin blocking antibody, CSAT, integrin/matrix interactions were disrupted. Results indicated that viability of both corneal fibroblasts and periocular mesenchyme cells was greater on type VI collagen than on type I collagen or BSA-blocked glass. In addition, less apoptosis was observed for both cell types on type VI collagen when β₁integrin–matrix interactions were disrupted. These data indicated that these cells require intact β₁interactions with type I collagen and with BSA-coated glass controls to remain viable. Thus, type VI collagen may play a role in the rescue of corneal cells from anti-β₁integrin-induced apoptosis by increasing cell survival, probably via a non-β₁integrin-dependent mechanism.