The interaction alters the electrochemical properties of the local membrane microdomain to permit dendritic spine elongation, synaptogenesis, and cell motility.113 In schizophrenia there is evidence of reduced total and pMARCKS,112 reduced polysialylation of NCAM,88,89,95 as well as reduced F-actin, increased globular (G) actin, and a reduced F-/G-actin ratio.116 Taken together, abnormal PTM status of either or both NCAM and MARCKS may alter the spatial dynamics of the PSA–MARCKS interaction and thereby contribute to abnormal dendritic spine morphology in this illness. The gene discussed is NCAM1; the disease is schizophrenia.