Speaker: Adam Antebi, PhD
Managing Director, Max Planck Institute for Biology of Ageing, Cologne, Germany
Time: 4:00-6:00 pm, Nov. 10（Friday）
Venue: Room 300, SIBS Main Building, Yueyang Road 320
Host: Prof. Jingdong Han
CAS-MPG Partner Institute for Computational Biology
Title: Convergent mechanisms of longevity
Research in model organisms over the last several decades has revealed that animal lifespan is plastic and regulated by conserved metabolic signaling pathways, which work through specific transcription factors to extend life. Whether these pathways affect common downstream mechanisms remains largely elusive. Our studies in C. elegans reveal that an extensive helix-loop-helix transcription factor network regulates life span across the major longevity pathways, and is interlinked via mTOR signaling. More recently, we have discovered that a major focal point of convergent regulation is the nucleolus. NCL-1/TRIM2/Brat tumor suppressor extends lifespan and limits nucleolar size in the major C. elegans longevity pathways. Animals representing distinct longevity pathways exhibit small nucleoli, and decreased expression of rRNA, ribosomal proteins, and the nucleolar protein fibrillarin, dependent on NCL-1. Fibrillarin is not only a marker but itself a causal factor whose knockdown reduces nucleolar size and extends lifespan. Among wild type C. elegans, individual nucleolar size varies, but is highly correlated for life expectancy; those with smaller nucleoli live longer, while those with larger nucleoli live shorter. Long-lived dietary restricted fruit flies and insulin-like-peptide mutants also exhibit reduced nucleoli and fibrillarin expression. Similarly, tissues derived from long-lived dietary restricted and reduced insulin/IGF signaling IRS1 knockout mice display reduced nucleoli. We suggest that small nucleoli are a cellular hallmark of longevity conserved across taxa.
All are welcome, and anyone who would like to have a talk with speaker, please feel free to contact Jing MU via email@example.com.