GEE Friday Seminar - Dr Kuei-Ching Hsiung, Postdoctoral Fellow, IHA

Abstract: It has been suggested that molecular damage accumulation is a predominant cause of ageing. Autophagy is a process whereby cellular constituents (including damaged ones) are broken down and recycled. One theory argues that autophagy slows ageing by preventing accumulation of molecular damage. Various findings support the view that autophagy is increased in daf-2 insulin/IGF-1 receptor mutants in C. elegans, and that this contributes to their extended lifespan. We previously found that age-related intestinal atrophy is promoted by wild-type IIS, and by autophagy, apparently supporting intestinal biomass repurposing into yolk. Moreover, IIS promotes protein turnover. These findings suggest that IIS promotes rather than suppresses autophagy. It is also consistent with emerging programmatic theories of ageing. To try to better understand the relationship between IIS, autophagy and ageing, we are re-examining effects of knockdown of genes encoding the machinery of autophagy on pathology and ageing, taking into consideration issues of timing and severity of knockdown, daf-2 allele class, temperature, bacterial status and other issues.