6^th Annual Conference on
Brain Disorders, Neurology and Therapeutics

Biography:

Haijun TU, Ph.D., a Professor of neuroscience, an assistant Dean of College of Biology, a director of International Science and Technology Cooperation Base of Biomedicine and Life Analytical Chemistry, Hunan University. He is He is currently a member of Society for Neuroscience and Chinese Neuroscience Society. His research interests are focusing on the molecular and cellular mechanisms of ischemia-induced Neuronal injury & Protection and Repairing and of neural regulation of innate immune response. He has published more than ten articles in the neuroscience field of journals such as Nature, Neuron, Journal of Neuroscience, EMBO Journal. He completed his postdoc training in the Bessereau laboratory of Génétique et Neurobiologie de C. elegans at University Claude Bernard Lyon1, CGphiMC UMR CNRS 5534, Lyon from July, 2013 to June, 2015 and in IBENS, INSERM U1024, Ecole Normale Supérieure, Paris, France from January, 2011 to June, 2013. Dr. Tu received his Ph.D. degree at Huazhong University of Science & Technology in 2008, received his master’s degree at Wuhan University in 2004. He received the award of Les Grandes Avancees Francaises en Biologie, Pix AXA – Academie des sciences in 2015.

Abstract:

Positioning neurotransmitter receptors in front of neurotransmitter release sites sets the excitability of neuronal networks. We previously identified an original synaptic organizer, Punctin/MADD-4, that specifies cholinergic versus GABAergic identity of post-synaptic domains at the NMJs. Punctin is secreted by the two types of motor neurons and localizes at NMJs. Alternative promoters generate different isoforms with different functions. In brief, the long Punctin isoform secreted by cholinergic motor neuron specifically localizes acetylcholine receptors at excitatory synapses, while the short Punctin isoform secreted by both cholinergic and GABAergic motoneurons is required for the proper localization of GABA_A receptor at inhibitory synapse. We also showed that Punctin controls the clustering of GABA_ARs through the synaptic adhesion molecule neuroligin (NLG-1) and the netrin receptor UNC‑40/DCC (Deleted in Colorectal Cancer). Punctin constitutes a new ligand of NLG-1/neuroligin and UNC-40/DCC and functions as a central anterograde organizer of inhibitory synapses. Since the mammalian orthologs of these genes are expressed in the central nervous system and their mutations are implicated in neuropsychiatric diseases, this novel molecular pathway might have been evolutionarily conserved. Moreover, we found that deficiency of GABAergic synapse promotes intestinal innate immunity of C. elegans through downregulating muscular insulin like peptide INS-31, suggesting a potential target for therapy of neuropsychiatric or/and innate immunity-related diseases. The data in details will be presented at the meeting.