Alex Theos

After graduating from Cambridge University with a degree in Natural Sciences, Alex stayed in Cambridge as a graduate student in the Department of Clinical Biochemistry under the supervision of Dr. Margaret (Scottie) Robinson. In Scottie’s lab he was interested in the role of ubiquitously-expressed cytoplasmic AP-3 adaptor protein complexes in the biogenesis of specialized organelles. He focused on the melanosome, a lysosome-related organelle that is the intracellular site of synthesis and storage of mammalian melanin pigments. Partially albino human patients suffering from a sub-type of the autosomal-recessive multisystem disorder Hermansky-Pudlak Syndrome (HPS) carry mutations that result in non-functional AP-3 complexes. After receiving his doctorate in 2002, Alex left the U.K. for a postdoctoral fellowship in the Department of Pathology and Laboratory Medicine in the School of Medicine at the University of Pennsylvania. His postdoctoral research, conducted under the mentorship of Dr. Michael Marks, built upon his graduate experience of the pigment cell system focusing on the intracellular membrane trafficking pathways followed by melanocyte-specific integral membrane protein cargoes including tyrosinase and Pmel17. Before joining the faculty as Assistant Professor of Human Science in 2007, he spent a year as a Visiting Assistant Professor at Swarthmore College in the Department of Biology. His current research interests include understanding the cell biology of the GPNMB gene product, a relative of the melanocyte-specific Pmel17 that is more ubiquitously expressed. Mice that lack Gpnmb expression develop pigmentary glaucoma in addition to bone defects. Undergraduate research assistants under Alex's mentorship are also studying the biology of other integral membrane protein cargoes that are delivered to specialized lysosome-related organelles, including tyrosinase and the related TYRP-1 protein. Very recently, his laboratory has initiated projects that seek to validate candidate drug targets for CRMO, a rare autoinflammatory disease of the bone.