生命科学联合中心
学术报告
Title：Reactive Oxygen Species regulate aging as signaling molecules
Speaker： Siegfried Hekimi, Ph.D
Department of Biology
McGill University, Montreal
Fellow of the Royal Society of Canada
Time：2018-4-17（周二），13:00 -14:00 pm
Venue：邓佑才报告厅，北京大学金光生命科学大楼
Host：刘颖&徐成冉，北大-清华生命科学联合中心
Abstract：
The oxidative stress theory of aging proposes that damage from reactive oxygen species (ROS) are the cause of aging. However, using the nematode Caenorhabditis elegans and mice, we have provided much evidence that this is not the case, including evidence that shows that mutants and treatments that increase mitochondrial ROS (mtROS) generation increase the longevity of C. elegans. Our working model is that ROS levels correlate with aging because ROS act to combat aging by modulating signal transduction pathways that promote survival. For example, we have shown that the pro-longevity action of ROS requires the intrinsic apoptotic signaling pathway in a manner that is completely independent of cell death. We are now successfully focusing on identifying the redox-sensitive cysteines in signaling proteins that are the targets of pro-longevity ROS signaling. We test the in vivo relevance of these residues for longevity by using CRISPR to replace them with either oxidation-resistant amino acids, or amino acids that mimic oxidized cysteines. With this approach we have been able to demonstrate that pro-longevity ROS act as genuine signaling molecules, and do not act by inducing an oxidative damage-dependent stress response.
