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Tarik F. Haydar, PhD
Children's National Medical Center
Children’s Research Institute (CRI)
Principal Investigator, Center for Neuroscience Research (CNR)

George Washington University
School of Medicine and Health Sciences
Assistant Professor, Pediatrics, Pharmacology and Physiology


Contact Information
Children's National Medical Center
Center for Neuroscience Research (CNR)
111 Michigan Avenue, NW
Washington, DC 20010-2970

202-476-2383
thaydar@cnmc.org


Education & Training
Institution & Location Degree Year(s) Field of Study
University of Massachusetts, Amherst, MA BS 1992 Microbiology
University of Maryland School of Medicine,
(Laboratory of Dr. Bruce Krueger)
College Park, MD
PhD 1997 Physiology
Yale Medical School
(Laboratory of Dr. Pasko Rakic), New Haven, CT
1997-2001 Postdoctoral Fellow
Yale University, Department of Neurobiology, New Haven, CT 2001-2002 Associate Research Scientist


Research Interests
Tarik Haydar, PhD, an internationally recognized expert in the field of cerebral cortical development, is an assistant professor in Pediatrics and Pharmacology, at the George Washington School of Medicine and a principal investigator in the Center for Neuroscience Research at Children’s National Medical Center in Washington, DC. Dr. Haydar is also the co-director of the Cellular Imaging Core in the Mental Retardation Disabilities Research Center at Children’s National. Dr. Haydar joined the staff at Children’s National in 2002. He came from Yale University, where he was a postdoctoral fellow and associate research scientist in the laboratory of Dr. Pasko Rakic. He earned his PhD in Physiology at the University of Maryland Medical School in Baltimore, where he studied prenatal development of the Ts16 mouse model of Down syndrome with Dr. Bruce Krueger. Dr. Haydar completed his undergraduate degree in Microbiology at the University of Massachusetts in Amherst where he studied RNA recombination in viruses. A cellular and molecular neurobiologist by training, Dr. Haydar has worked through his career to define the molecules and cellular mechanisms responsible for cerebral cortical development. He uses state-of-the-art imaging tools to assay cortical development using time-lapse microscopy, and is also extending his previous work on cortical development in Down syndrome studying both mouse model and human embryonic development. He has published more than 20 articles and 18 abstracts.
Left: This image illustrates 48 hours of development in an embryonic day 15 (E15) mouse brain. The VZ progenitor cells were labeled with a GFP expression vector on E13. In the subsequent two days, neurons born from the VZ and SVZ progenitors migrate out through the intermediate zone (IZ) to the cortical plate (CP). Once in the CP (the future cortical grey matter), neurons find their proper layer and begin to establish synaptic circuits.

Laboratory Members
Mitali Chatterjee, Technician
Sophia Smith, Clinical Fellow
Jonathan Gal, Graduate Student

During embryonic development, a pool of rapidly dividing stem cells generates the complex architecture and function of the mammalian cerebral cortex. Understanding the molecular signals that control this process is a fundamental goal of developmental neurobiology. Dr. Haydar’s work is aimed at understanding how growth of the cerebral cortex is controlled in both wild-type mice and mutant mouse models of disease. His team is particularly interested in the multiple progenitor cell types in the neocortical ventricular zone (VZ) and the factors that control their division and lineage progression during the course of development. Dr. Haydar pursues these issues using a variety of cellular, molecular, and imaging techniques. In particular, he has a special focus on real-time analysis of molecules using in utero gene transfection and multiphoton imaging. The laboratory runs and maintains an LSM510 META NLO microscope from Carl Zeiss, Inc.

The number and diversity of cells in the cerebral cortex is due, in great measure, to the mode of VZ progenitor cell division before birth. Symmetrical founder cell divisions, which predominate early, yield more progenitors and lead to an exponential expansion of the VZ population. In contrast, asymmetrical divisions, which prevail during later stages of neurogenesis, lead to cell commitment and diversity of the cortical architecture. Thus, the switch between symmetrical and asymmetrical divisions has to occur properly for the cortex to develop normally. Despite the importance of this developmental strategy for brain growth, it is unknown how conversion between these major types of mitotic divisions is achieved in the VZ of the mammalian forebrain.
Right: A living organotypic slice of an E12 mouse neocortex stained with Cell Tracker Green and SYTO 82 (Molecular Probes). Note the dividing VZ cell (bottom center).
Right: The morphology of transfected VZ cells is elucidated by this 3D reconstruction. This confocal image stack was taken from a brain transfected with GFP driven by the Ta1 promoter (click image to download the ~18MB QuickTime movie).
Right: This image illustrates 48 hours of development in an embryonic day 15 (E15) mouse brain. The VZ progenitor cells were labeled with a GFP expression vector on E13. In the subsequent two days, neurons born from the VZ and SVZ progenitors migrate out through the intermediate zone (IZ) to the cortical plate (CP). Once in the CP (the future cortical grey matter), neurons find their proper layer and begin to establish synaptic circuits.

Left: In utero transfection of dividing VZ cells with EGFP and 3D reconstruction elucidates multiple cell types (long, arrows; short, arrowheads).

Dr. Haydar’s recent work suggests that the mode of division is in part regulated by rotation and alignment of the mitotic spindle prior to anaphase. Using time-lapse multiphoton imaging of organotypic slices, it was determined that symmetrical divisions occur rapidly with littlespindle rotation while asymmetric cleavages proceed slowly only after considerable spindle rotation. Major goals in Dr. Haydar’s lab are now 1) to investigate how the spindle rotation is controlled in dividing VZ cells, 2) to determine how this spindle rotation partitions fate specifying molecules into daughter cells upon division, and 3) to determine the roles of different VZ cell types during neocortical development.


Publications
View a partial list of Tarik F. Haydar's publications through the National Library of Medicine's PubMed online database.


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