"issecting the molecular and genetic mechanism of mental retardation"张永清 博士（中科院遗传发育生物学研究所）-2010.10.8

时间：2010年10月8日 10:00

地点：脑功能重点实验室一楼会议室

报告人：张永清 博士 中科院遗传发育生物学研究所

报告题目：issecting the molecular and genetic mechanism of mental retardation

报告人简介：张永清，中科院遗传与发育生物学研究所研究员。1991年获北京农业大学（现中国农业大学）博士学位，先后在中国科学院微生物研究所、荷兰Wageningen大学、英国剑桥大学、美国尤他大学和Vanderbilt大学作博士后和访问学者。获得美国FRAXA Research Foundation（2001-2002）和 Vanderbilt大学Kennedy Center for Research on Human Development（2003）的研究奖。2004年中国科学院“百人计划”入选者，2005年国家杰出青年科学基金获得者。主要研究方向为以果蝇为模式动物研究人类重要神经疾病包括智力低下的分子遗传机制，从而为这类疾病的预防和治疗提供理论依据，同时为神经系统的正常发育和功能提供新的见解。

报告简介：Mental retardation (MR, also known as intellectual disability) is present in 1–3% of the general population and is a complex phenotype characterized by suboptimal brain function with onset before the age of 18. MR is divided into syndromic and non-syndromic forms depending on whether MR is associated with other anomalies. Fragile X syndrome, the most common form of inherited mental retardation, is caused by the absence of the fragile X mental retardation protein FMRP. The RNA-binding FMRP represses translation of the microtubule-associated protein 1B (MAP1B) during synaptogenesis in the brain of the neonatal mouse. However, the effect of FMRP on microtubules remains unclear. Mounting evidence shows that the structure and function of FMRP are well conserved across species from Drosophila to human. Due to the powerful genetics, the simple anatomy of the nervous system, and a large array of morphological and functional assays available in Drosophila melanogaster, commonly known as fruitflies, we have been using the model organism to dissect the molecular and genetic mechanism of MR for the last decade. I’ll discuss two new findings in my laboratory implicating microtubule cytoskeleton and axonal transport in MR.