My research revolves around the role of the gamma-protocadherins in the choroid plexus (CP) epithelium. The CP is the main contributor to cerebrospinal fluid (CSF) production, which is critical for brain health and homeostasis. The CP comprises four epithelia, each residing in one of the ventricles of the brain. This tissue expresses the gamma-protocadherin family of cell adhesion molecules extremely highly, and localizes the proteins strictly to its apical surface, where they presumably have little to bind. Thus, we want to understand the role that the gamma-protocadherins are playing in this important tissue, which may include mechanisms distinct from their cell-interaction functions.  Interestingly, removing these proteins from the choroid plexus (by restricted gene knockout in mice) results in cerebral ventricular atrophy. This atrophy does not appear to be a result of cell morphology or developmental defects, and appears to be a reflection of reduced CSF production.  To determine the mechanisms underlying this phenotype, I am investigating gene expression of the CP between mutants and controls using Nimblegen transcriptome arrays, to identify alterations that could be responsible for the observed ventricular atrophy. I am also investigating a possible immunosurveillance role for the gamma-protocadherins in the choroid plexus, as I have found that leukocytes also express these genes. As the CP is known to be a major site of lymphocyte entry into the CNS following inflammation, uncovering a role for the gamma-protocadherins in this process may have important human health implications. 

Recent publications