报告题目： Study of autism-linked genes in synaptic function

时间: 2017年6月16日 上午10:00

地点： 中北校区 脑功能基因组学研究所一楼会议室

报告人🪻： 童夏静 博士 

主持人： 殷东敏 研究员

 

报告人简介: 童夏静 博士，Research Associate🙆🏻‍♂️，美国哈佛医天美。2010年在中科院生物化学与细胞生物学研究所获得生化与遗传学博士学位😹，后赴美国哈佛医天美神经生物学系进行博士后研究（Joshua Kaplan 博士实验室），2016年升任Research Associate至今🩲👨🏼‍🦳。主要研究方向为自闭症的分子神经机制，其研究成果发表于Neuron、Elife、Nature Structural & Molecular Biology 等学科领域的高影响杂志。

 

报告简介：Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by impairments in social skills, difficulties in communication, and restricted repetitive behaviors. Despite the increasing prevalence in past decades, effective medications to cure ASD are still lacking. ASD has strong genetic basis. Extensive genome sequencing and screening as well as numerous following studies have revealed the impaired synaptic function as a major contributing factor in ASD. However, the detailed molecular mechanisms underlying synaptic dysfunction are not well understood. We study two aspects of synaptic function that have been implicated in the pathophysiology of ASD: inhibitory synaptic transmission and homeostatic synaptic plasticity using C. elegans neuromuscular junction (NMJ) as our model system. First, we found that inhibitory synapses contain the immobile and diffusing pools of GABAA receptors that are stabilized by distinct scaffolds encoded by ASD-linked genes. Second, we revealed molecular mechanisms of synaptic retrograde inhibition signaling that is critical for homeostatic synaptic plasticity. In summary, we identified a network of autism-linked genes that regulate inhibitory synapse receptors stabilization and excitatory synapse homeostasis maintenance.