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Senior Scientist, Regenerative Medicine, Ottawa Hospital Research Institute
Associate Professor, Department of Biochemistry, Microbiology, and Immunology, Faculty of Medicine, University of Ottawa
Dr. Picketts completed a PhD at Queen's University (Kingston) with Dr. David Lillicrap studying the transcriptional regulation of the Factor IX gene. He then pursued postdoctoral research in Oxford, England with Dr. Douglas Higgs at the Institute of Molecular Medicine. With another research fellow, Dr. Richard Gibbons they identified the ATRX gene as the cause of the ATR-X syndrome, a severe form of X-linked intellectual disability (XLID). They cloning of the ATRX gene established the paradigm that dysfunctional chromatin remodeling proteins cause human disease, specifically neurodevelopmental disorders. Dr. Picketts has extended his research to explore the role of three other chromatin-interacting proteins in disease and brain development including PHF6 and the ISWI proteins, SNF2H and SNF2L. In his spare time, Dr. Picketts remains an avid ice hockey enthusiast playing and coaching several times a week and he is an alumni of the Oxford Ice Hockey Team.
- ATP-dependent chromatin remodeling, Brain development, Intellectual disability, Heterochromatin maintenance.
Major Research Activities
Chromatin remodeling proteins and XLID: Chromatin remodeling proteins play a dynamic role in the regulation of gene expression through the alteration of nucleosome structure (histone acetylation, phosphorylation and methylation) or the ATP dependent repositioning of nucleosomes (SWI/SNF complex, ISWI). Their involvement in genetic disease was established by our cloning of the ATRX gene, a novel SWI/SNF family member that is mutated in a severe X-linked intellectual disability syndrome usually associated with alpha thalassemia. This paradigm has since been extended to include genes encoding almost every type of chromatin modifying protein (see Table 1). We continue to study the role of these proteins in neural development to understand how they contribute to disease pathogenesis.
forebrain development, chromatin remodeling, neurodevelopment, intellectual disability, TRRX, ISWI, PHF6, autism spectrum disorders, ATR-X syndrome, Borjeson-Forssman-Lehmann syndrome, Rett syndrome