Department of Cell Biology, Emory University
Our laboratory is interested in the molecular mechanisms underlying schizophrenia. Multiple neurodevelopmental and neurochemical pathogenic hypotheses have been proposed, each of which is based on a limited set of abnormalities found in the disorder. Epidemiological genetics has identified multiple genes associated with schizophrenia susceptibility. Among these, the gene encoding dysbindin, DTNBP1, stands out as a top-ranking disease susceptibility gene. The cellular and molecular mechanisms that require dysbindin function in neurons are mostly unexplored and they constitute the main focus of our laboratory. We hypothesize that dysbindin-dependent endosome trafficking to and from the plasma membrane controls the subcellular localization of membrane proteins whose genes are associated with schizophrenia risk. This hypothesis is founded on the observation that defects in the dysbindin/BLOC-1 pathway lead to increased surface levels of plasma membrane neurotransmitter receptors and aberrant neurotransmission, including impaired homeostatic synaptic plasticity. Our laboratory is testing fundamental predictions derived from this hypothesis using a combination of mouse genetics, cellular, and molecular approaches in neuronal cells.
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