学术报告
报告题目：Genome maintenance by the 9-1-1 DNA damage checkpoint complex during mammalian development and tumorigenesis
报告人：Robert S. Weiss, Ph.D.
Associate Professor
Department of Biomedical Sciences
Cornell University
时间: 2012年2月28日（周二）上午10点
地点: 新生物楼411室
联系人：方敏（电话：62768106）
Eukaryotic cells continuously experience DNA damage that originates from both intrinsic and extrinsic sources. If left uncorrected, the resulting genomic lesions can result in developmental defects, premature aging, and increased cancer risk. Cells protect against these undesirable outcomes using a variety of mechanisms, including DNA damage checkpoint pathways that promote DNA repair and coordinate repair processes with cell cycle progression. The Weiss laboratory uses mouse models to investigate mammalian genome maintenance mechanisms and the physiological consequences of genomic instability. A primary research objective is to understand the functions of the essential checkpoint protein Hus1, a component of the heterotrimeric 9-1-1 complex that promotes DNA damage-induced checkpoint signal transduction and also directly participates in DNA repair by recruiting repair proteins to DNA lesions. The presentation will focus on new mouse models that bypass the severe phenotypes associated with germline Hus1 inactivation and their use in analyzing the impact of checkpoint dysfunction on organismal development, tumorigenesis, and DNA damage responses in adult mice.
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