Dawson research group 2015

Dawson research group 2015

Dawson research group 2015


Our Mission is to promote the idea that sphingolipids control the organization of signaling protein molecules in membranes and that many diseases can be explained by defects in their metabolism. WHAT WE DO

Lipid rafts organize membranes


View Dr. Glyn Dawson's PUBLICATIONS

  • The research emphasis of the Dawson Lab is to understand the role of sphingolipids in how our brains work.  Sphingolipids play critical roles in brain development, myelination, cancer and many types of neurodegeneration.
  • Our model systems are mice deficient in key enzymes, primary cultures of neurons, oligodendrocytes and astrocytes as well as cell lines derived from patients with genetic diseases. 
  • Our techniques include chromatography, mass-spectrometry, confocal microscropy, DNA manipulation and a range of biochemical and genetic approaches. 
  • Our goal is to develop novel drugs and new types of nanotechnology in which nanoparticles (Quantum dots) deliver drugs to the central nervous system to repair neurodegeneration. 
  • This will help us better understand and treat lysosomal storage diseases which cause mental retardation (such as Batten disease) as well as many human neurodegeneratve diseases such as Multiple Sclerosis and Parkinsons disease.  What is most exciting is that sphingolipids form microdomains in the plasma membrane which regulate many types of cell signaling. This dynamic process is what drives the brain and where most of the problems occur which result in human disease.


Philip Dawson, PhD., The Scripps Institute, San Diego, CA  http://www.scripps.edu/dawson/



Luminescent semiconductor nanocrystals or quantum dots (QDs) are a potent prototypical nanoparticulate material whose intrinsic physiochemical and optical properties have much to offer for understanding the mechanisms underlying the growing field of nanoparticle mediated drug delivery.  Here, we evaluate the potential role of CdSe/ZnS core/shell QDs surface functionalized with a compact zwitterionic ligand in delivering peptide to the developing chick embryo brain. To achieve this, functionalized QDs were conjugated to the palmitoylated peptide WGDap(Palmitoyl)VKIKKP9GGH6, which facilitates endosomal escape, and microinjected into the embryonic chick spinal cord canal at embryo day 4 (E4).  We observed extensive labeling of spinal cord which extended into the ventricles, migratory neuroblasts, maturing brain cells and structures.  QD intensity peaked between E8 and E11 where we observed intense QD fluorescence in recently developed structures such as the choroid plexus.  After this time, visible QD labeling declined significantly until hatching (E21/P0).  We observed no abnormalities in embryonic patterning or survival, and mRNA in situ hybridization confirmed that at key developmental stages, the expression pattern of genes associated to different brain cell types (brain lipid binding protein, Sox-2, proteolipid protein and Class III-b-Tubulin) all showed a normal labeling pattern and intensity.  Overall, our findings suggest several exciting possibilities concerning the use of QDs and other nanoparticles in brain developmental models. These include: identifying and tracking neural stem cells with QDs as they migrate; demonstrating that the choroid plexus is a mechanism for clearing injected QDs/nanoparticles from the brain after E11, and delivering a drug or peptide/protein cargo via a nanoparticle to most parts of the developing brain.