SPEAKER: Ziyun Wu Tenure-track Associate Professor; Ph.D.; Supervisor PI Department of Food Science & Engineering，SAB   Research Interests Why are we aging? Why does aging cause a lot of diseases? Can we slow aging? These are some of the greatest unsolved questions in biology. Aging and anti-aging is now a fast-developing field. My research interesting focuses on study of biological aging. Specifically, I aim to explore the following three research areas: (1) Nutrients and longevity; (2) Innate immunity and aging; (3) Metabolism and aging. I have a dream that one day I can develop a powerful longevity food product for human.

TIME ：12:45-13:30  Dec 9, 2020  (Wednesday)

VENUE：Room 104, Building B, School of Agriculture and Biology

ORGANIZER：Office of Discipline and Science & Technology, SAB; Young Teachers Association, SAB

TITTLE: Food intake, innate immunity and longevity

ABSTRACT: 

An important hallmark of human aging is immune dysregulation.  Aging increases chronic innate immune activity and inflammation, a major risk factor for age-related pathologies that include diabetes, cancer, and neurodegenerative and cardiovascular disease. The emerging idea that innate immunity is influenced by metabolic activity is of great interest, because of the potential importance in metabolic disease, but it is unknown whether immunity regulation might be important for extending healthy lifespan.  Here we show that in C. elegans, dietary restriction (DR) extends lifespan by modulating a conserved innate immunity pathway that is regulated by p38 signaling, and the transcription factor ATF-7.  Longevity from DR depends upon p38–ATF-7 immunity being intact, but downregulated to a basal level.  p38–ATF-7 immunity accelerates aging when hyperactive, influences lifespan independently of pathogen exposure, and is activated by nutrients independently of mTORC1, a major DR mediator.  Longevity from reduced insulin/IGF-1 signaling (rIIS) also involves p38–ATF-7 downregulation, with signals from DAF-16/FOXO reducing food intake.  We conclude that p38–ATF-7 is an immunometabolic pathway that senses bacterial and nutrient signals, that immunity modulation is critical for DR, and that DAF-16/FOXO couples appetite to growth regulation.  These conserved mechanisms may influence aging in more complex organisms. An understanding of how the p38–ATF-7 pathway is regulated by nutrients and bacterial signals, and feeding by DAF-16, may therefore reveal new possibilities for influencing human appetite, immunity, and longevity.