A novel pathway regulates social hierarchy via lncRNA AtLAS and postsynaptic synapsin Ⅱb  

作　　者：Mei Ma Wan Xiong Fan Hu Man-Fei Deng Xian Huang Jian-Guo Chen Heng-Ye Man Youming Lu Dan Liu Ling-Qiang Zhu 

机构地区：[1]Department of Pathophysiology,School of Basic Medicine,Tongji Medical College,Huazhong University of Science and Technology,Wuhan,Hubei 430030,China [2]The Institute of Brain Research,Collaborative Innovation Center for Brain Science,Huazhong University of Science and Technology,Wuhan,Hubei 430030,China [3]Department of Biology,Boston University,Boston,MA 02215,USA

出　　处：《Cell Research》2020年第2期105-118,共14页细胞研究（英文版）

基　　金：Supported partially by the National Natural Science Foundation of China(81871108,81829002,81961128005,81761138043,91632114,81771150,31571039,31721002),Top-Notch Young Talents Program of China of 2014,and Academic Frontier Youth Team of Huazhong University of Science and Technology to L.Q.Z.

摘　　要：Dominance hierarchy is a fundamental phenomenon in grouped animals and human beings,however,the underlying regulatory mechanisms remain elusive.Here,we report that an antisense long non-coding RNA(lncRNA)of synapsinⅡ;named as AtLAS,plays a crucial role in the regulation of social hierarchy.AtLAS is decreased in the prefrontal cortical excitatory pyramidal neurons of dominant mice;consistently,silencing or overexpression of AtLAS increases or decreases the social rank,respectively.Mechanistically,we show that AtLAS regulates alternative polyadenylation of synapsinⅡgene and increases synapsin 2b(syn2b)expression.Syn2b reduces AMPA receptor(AMPAR)-mediated excitatory synaptic transmission through a direct binding with AMPAR at the postsynaptic site via its unique C-terminal sequence.Moreover,a peptide disrupting the binding of syn2b with AMPARs enhances the synaptic strength and social ranks.These findings reveal a novel role for lncRNA AtLAS and its target syn2b in the regulation of social behaviors by controlling postsynaptic AMPAR trafficking.

关 键 词：expression. POSTSYNAPTIC AMPA 

分 类 号：Q42[生物学—神经生物学]