AGEP-T FRAME Fellow: Azeez Aranmolate
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Azeez Aranmolate Graduate Student, Stony Brook University Department of Molecular & Cellular Biology AGEP-T FRAME Research Mentor: Dr. Holly Colognato |
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Born in U.S.A to Nigerian and Trinidadian parents, I spent 6 years of my childhood in Nigeria. I enjoy movies, food & traveling, as exhibited by trips to Jamaica, France, Italy, England, Canada, Guatemala and Vietnam. In the past, I volunteered as a Fireman/EMT and worked as a pharmacy technician and associate scientist in biotech. Currently, I am a PhD student in a Molecular and Cellular Biology program, with a chosen specialty in Immunology and Pathology. My dissertation lab however, belongs to the Pharmacology Department and focuses on Neuropharmacology (both glial development and degeneration). Due to the multifaceted nature of my PhD, I want a career at agencies working on topics related to a variety of diseases, from neurodegenerative disease to cancer to infectious disease. Seminar Title: A Role for Duchenne Muscular Dystrophy Gene in Central Nervous System Myelination Description: Along with severe muscle atrophy, Duchenne muscular dystrophy (DMD), which is caused by mutations in the dystrophin gene, also results in attention/learning disabilities, seizures and other kinds of cognitive impairments; however, the cellular dysfunction triggering these brain impairments remains unknown. Myelination is critical for the speed and coordinated timing required for all complex nervous system function, however, it also remains unknown if oligodendrocytes, the myelinating cells of the brain, contain dystrophin, and if so, whether it is required for normal oligodendroglial development. Here we will determine if oligodendrocytes have both dystrophin and an associated dystrophin-associated glycoprotein complex (DGC) that contribute to successful myelination and brain function. The multi-subunit Dystrophin Glycoprotein Complex (DGC) is crucial in maintenance of skeletal muscle membrane stability. In Duchenne Muscular Dystrophy (DMD), the genetic loss of the dystrophin component of the DGC compromises the DGC's ability to maintain muscle membrane integrity, thereby causing muscle atrophy. Furthermore, DMD patients also experience brain deficits of unknown cellular etiology. Previous studies on dystrophin and its associated DGC have primarily focused on muscle and select non-muscle tissues such as liver, retina, kidney and brain (neurons, astrocytes). Our recent studies also reveal that the dystroglycan component of the DGC is present in oligodendrocytes, the myelinating cells of the brain, and it is required for normal oligodendroglial development. Yet, it remains unknown if oligodendrocytes also possess dystrophin or a DGC that contribute to successful myelination and brain function. In the proposed study, we aim to address this issue by characterizing the components and spatial/temporal regulation of a putative oligodendroglial DGC during brain myelination. In addition, we will also determine if dystrophin regulates oligodendroglial development and myelination during brain development via a mechanism that involves nuclear translocation of a dystrophin-dystroglycan complex. Ultimately, this study aims to illuminate the underlying basis of DMD associated brain defects, and potentially shed light on novel therapeutic approaches. Publications: Menezes, M.J., McClenahan, F.K., Leiton, C., Aranmolate, A., Shan, X., and Colognato, H. The extracellular matrix protein laminin alpha2 regulates the maturation and function of the blood-brain barrier. (2014) J. Neurosci., 34(46):15260 –15280 Leiton, C., Aranmolate, A.,Eyermann, C., Menezes, M.J., Escobar-Hoyos, L., Husain, S., Winder, S., and Colognato, H. Laminin promotes metalloproteinase-mediated dystroglycan processing to regulate proliferation in oligodendrocyte progenitor cells. (Accepted for publication by Journal of Neurochemistry on Jul 6, 2015) |
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