MOLECULAR MECHANISM UNDERLYING BRAIN ASYMMETRY AND AUTISM

The brain's hemispheres exhibit profound lateralization, yet the underlying mechanisms remain elusive. Analyses of the bilateral striatum, a hub for important brain functions and a common node of autism pathophysiology, reveals significant phosphorylation asymmetries. Notably, autism spectrum disorder (ASD)-related protein SH3RF2 forms a complex with CaMKII (an ASD-associated protein) and PP1. Loss of SH3RF2 disturbs the CaMKII/PP1 “switch”, resulting in impaired functional lateralization of striatal neurons and autism-like behavior. Therefore, it reveals for the first time the molecular mechanism governing brain lateralization in mammals and links it to the development and treatment strategies of autism.

Biography
Zhiheng Xu, M.D., Ph.D., senior PI, former director of the Center for Molecular Development at the Institute of Genetics and Developmental Biology, Chinese Academy of Sciences. He received his Ph.D. from Rutgers University in 1999. From 1999 to 2005, he worked as a postdoctoral fellow/research associate at Columbia University. His research focuses on brain development and disease mechanisms. Over the past decade, he has published over 50 papers as corresponding author in journals such as Science, Cell Stem Cell, Nature Neuroscience, Immunity, Nature Metabolism, Nature Communications (5 papers), Cell Reports (5 papers), PNAS (4 papers), J Cell Biology, Cell Research (5 papers) etc. The total impact factor of his papers is >1000, and the citations are >9500 times.