Patient-derived cells were less adhesive and more motile than cells derived from healthy controls and their motility was reduced to control cell levels by integrin-blocking antibodies and by inhibition of focal adhesion kinase. Vinculin-stained focal adhesion complexes were significantly smaller and fewer in patient cells. Time-lapse imaging of cells expressing focal adhesion kinase tagged with green fluorescent protein revealed that the disassembly of focal adhesions was significantly faster in patient cells. The evidence for altered motility and focal adhesion dynamics in patient-derived cells is consistent with dysregulated gene expression in the focal adhesion kinase signalling pathway in these cells. Alterations in cell adhesion dynamics and cell motility could bias the trajectory of brain development in schizophrenia.
