北京大学 | ENGLISH
讲座信息
Posttranslational and epigenetic regulation of Hedgehog and Notch signaling in development
发布时间:2012-07-04      点击量:1613
主讲人:Alan Jian Zhu
讲座地点:生命科学学院610会议室
讲座日期:2012-07-23
 
学术报告
题目:Posttranslational and epigenetic regulation of Hedgehog and Notch signaling in development
报告人:Alan Jian Zhu, Ph.D.
Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation;
Departments of Genetics and Molecular Medicine, Case Western Reserve University School of Medicine
时间: Monday 10:00 a.m., July 23rd
地点:生命科学学院610会议室
Signal transduction systems, such as Hedgehog (Hh), Notch, Wnt and growth factor signaling, are repeatedly utilized in animal development to coordinate cell fate decisions, tissue patterning and organ growth. Despite tremendous efforts in uncovering essential components of the signaling cascades and basic principles of how they operate, very little is known as to how developmental signals are produced and interpreted, two fundamental questions in development. My laboratory utilizes Drosophila wing development as a model system to address these two questions. In the first part of my seminar, I will describe a molecular mechanism by which cells utilize to interpret development signals. We found that differential phosphorylation of Smoothened (Smo) protein, an essential activator of Hh signaling, converts the concentration thresholds of Hh signals into a graded signaling activity. I will also discuss how the spectrum of differential Smo phosphorylation is established and maintained by phosphatase activities. In the second part of my seminar, I will describe a molecular mechanism that controls the production of core components of developmental signaling. We identified a novel gene, stuxnet, which plays an essential role in the transcription of the Notch receptor gene. Stuxnet protein destabilizes Polycomb protein, an essential component of the Polycomb Repressive Group complex 1 (PRC1), thereby reducing the repressive chromatin modification marker imposed on the Notch receptor locus. We named this gene stuxnet after the powerful virus that destroys PC computers. Our work uncovered a novel mechanism for the control of the activity and stability of the PRC1 transcriptional silencing machinery in development.
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