Abstract：

The ability of the nervous system to coordinate organismal-wide mitochondrial proteostasis is essential for whole-body fitness under stress conditions and during aging. Our work discovered that neuronal mitochondrial stress can be sensed and responded to by the distal tissue via a secreted Wnt signal, resulting in lifespan extension in  C. elegans . Recently, we further identified two sensory neurons that coordinate the systemic mitochondrial stress response and various physiological characteristics in peripheral tissues via GPCR signaling pathways. More importantly, the neuronal mitochondrial stress can also communicate to the germ cells, which promotes the maternal inheritance of elevated levels of mitochondrial DNA (mtDNA), thereby passing down a “stress memory” to offspring, enabling descendants with a greater tolerance to stress and a longer lifespan. Together, these results open new avenues of research to explore inter-tissue mitochondrial stress signaling communication. Understanding of how the mitochondrial stress pathways may impinge upon the aging process will ultimately promote the development of therapeutic targets to promote mitochondrial function and combat age-related neurodegenerative diseases.

简介：

田烨，中国科学院遗传与发育生物学研究所研究员，博士生导师。2005年毕业于北京师范大学，获学士学位；2010年获北京生命科学研究所（NIBS）与北京师范大学联合培养，分子生物学与生物化学专业博士学位；2010-2016先后在美国Salk研究所和加州大学Berkeley分校进行博士后研究。2016年加入中科院遗传发育所，实验室聚焦线粒体应激和衰老调控的机制研究。利用线虫、细胞和小鼠等模式生物，探索线粒体稳态维持与修复机制，及其在衰老与衰老相关神经退行性疾病中的作用机理。以通讯或第一作者身份在Cell（2010，2016，2018）、Nature Cell Biology（2021）、Developmental Cell（2022）、Cell Reports（2022）、Science Advances（2020）、Trends in Biochemical Sciences（2022）等国际学术期刊发表多篇论文和综述。获得国家杰出青年科学基金，国自然重点项目资助，曾主持科技部重点研发计划青年项目。荣获中源协和生命医学-创新探索奖，中国动物学会青年科技奖。