Huaiyu Hu, PhD
- Associate Professor of Neuroscience and Physiology
- Associate Professor of Neuroscience Graduate Program
Research Programs and Affiliations
- Biomedical Sciences Program
- Cancer Research Institute
- Neuroscience Program
- Neuroscience and Physiology
- Physiology Program
- Research Pillars
- Molecular studies of brain malformations.
Migration of neurons from their birth place to their final locations is essential during development of the mammalian brain. Disorders of neuronal migration result in severe malformation and malfunctions of the human brain. Our laboratory is interested in the guidance mechanisms involved in the neuronal migration. We are currently working on two projects. One project focuses on Slit proteins and their roundabout receptors which are believed to be involved in the guidance several populations of neurons. We are studying how heparan sulfate regulates Slit signaling in cell migration and axon guidance. The other project concerns the roles of protein O-mannosylation in neuronal migration. Congenital muscular dystrophies with brain malformations such as Walker-Warburg syndrome, Fukuyama congenital muscular dystrophy, muscle-eye-brain diseases are caused by genetic mutations in genes involved protein O-mannosyl glycosylation. We are currently studying the cellular and molecular mechanisms of protein O-mannosylation in regulating brain development.
Hu H, Tomasiewics H, Magnuson T, Rutishauser U (1996) The role of polysialic acid in migration of olfactory interneuron precursors in the subventricular zone. Neuron 16(4):735-743.
Hu H, Rutishauser U (1996) A septum-derived chemorepulsive factor for migrating olfactory interneuron precursors. Neuron 16(5):933-940.
Hu H (1999) Chemorepulsion of neuronal migration by Slit2 in the developing mammalian forebrain. Neuron 23:703-711.
Hu H (2000) Polysialic acid regulates chain formation by migrating olfactory interneuron precursors. J Neurosc Res 61:480-492.
Hu H (2001) Cell surface heparan sulfate is involved in repulsive guidance activities of Slit2 protein. Nature Neurosci 4(7):695-701.
Liu J, Zhang L, Wang D, Shen H, Jiang M, Mei P, Hayden PS, Sedor JR, Hu H (2003) Congenital diaphragmatic hernia, kidney agenesis and cardiac defects associated with Slit3-deficiency in mice. Mech Dev 120:1059-1070.
Liu J, Ball SL, Yang Y, Mei P, Zhang L, Shi H, Kaminski HJ, Lemmon VP, Hu H (2006) A genetic model for muscle-eye-brain disease in mice lacking protein O-mannose beta1,2-N-acetylglucosaminyltransferase (POMGnT1). Mech Dev 123:228-240.
Hu, H. Yang, Y., Eade, A., Xiong, Y., and Qi, Y. Breaches of the Pial Basement Membrane and Disappearance of the Glia Limitans during Development Underlie the Cortical Lamination Defect in the Mouse Model of Muscle-eye-brain Disease. J. Comp. Neurol. 501(1)168-183, 2007.