"issecting the molecular and genetic mechanism of mental retardation"張永清 博士（中科院遺傳發育生物學研究所）-2010.10.8

時間：2010年10月8日 10:00

地點：腦功能重點實驗室一樓會議室

報告人：張永清 博士 中科院遺傳發育生物學研究所

報告題目：issecting the molecular and genetic mechanism of mental retardation

報告人簡介：張永清，中科院遺傳與發育生物學研究所研究員。1991年獲北京農業大學（現中國農業大學）博士學位，先后在中國科學院微生物研究所、荷蘭Wageningen大學、英國劍橋大學、美國尤他大學和Vanderbilt大學作博士后和訪問學者。獲得美國FRAXA Research Foundation（2001-2002）和 Vanderbilt大學Kennedy Center for Research on Human Development（2003）的研究獎。2004年中國科學院“百人計劃”入選者，2005年國家杰出青年科學基金獲得者。主要研究方向為以果蠅為模式動物研究人類重要神經疾病包括智力低下的分子遺傳機制，從而為這類疾病的預防和治療提供理論依據，同時為神經系統的正常發育和功能提供新的見解。

報告簡介：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.