"Genetic dissection of the neurodevelopmental function of thyroid hormone in tyhe mouse cerebellum"Frederic Flamant 博士-2014.12.5
发布时间:2014-12-05 

"Genetic dissection of the neurodevelopmental function of thyroid hormone in tyhe mouse cerebellum"Frederic Flamant  博士-2014.12.5

时间:2014年12月5日 10:00

地点:脑功能基因组学教育部重点实验室一楼会议室

报告题目:Genetic dissection of the neurodevelopmental function of thyroid hormone in tyhe mouse cerebellum

报告人:Frederic Flamant  博士

主持人:周晓明 教授

 

报告人简介:

1986:  Ph.D. in molecular and cellular biology. University of Lyon.  Research topic: « Use of avian leukosis retrovirus as vector for transgenesis ».
1986-1988: Post-Doctoral fellow Scripps Clinic San Diego. California USA. Research topic: Regulation of transcription of murine leukemia retroviruses. In vitro synthesis of infectious genomes.
1988-1990:  ENSA Rennes. Hired as Chargé de Recherche National Research Institute for Agronomy. Laboratory of Genetics. Research topic: Genetic determinism of adiposity in chicken.
1990-1998:  Laboratory of Molecular Biology of the Cell. Ecole Normale Supérieure de Lyon. Oncogenesis and Development group.  Position: CR1 INRA. Research topic: Gene transfer technology with avian retroviruses.
1998-2006:  Same group. New research topic : « Thyroid hormone receptors and development ». Collaboration on the generation of mouse models for sheep prion disease.
2006:  DR2 INRA Group leader at Institute for Functional Genomics in Lyon (IGFL). Neurodevelopment group. Research topics: Thyroid hormone receptors in brain development and adult brain function.

 

报告简介:Thyroid hormone (TH) exerts a broad influence on neurodevelopment by directly activating the transcription of genes regulated by the TRalpha and TRBeta nuclear receptors, present in all cell types. Rodent cerebellum has been a favorite model to investigate the associated cytological defects, which reflects impaired neuronal and glial cells differentiation. Among the known defects associated to TH deficiency, some are direct consequences of the lack of receptors activation, whereas others as secondary to a default in neurotrophins production. To unravel this complex situation, we used Cre/loxP technology in mice to generate somatic mutations of the genes encoding the TH nuclear receptors. This in vivo analysis was combined to a genome wide analysis of TH response performed in a neural cell line. As TH exerts its influence directly on gene expression,these approaches offer an original access to the basic genetic programs which underly normal neurodevelopment.