Maria E. Giannakou

TL;DR: When overexpressed, the NAD-dependent protein deacetylase Sir2 extends the lifespan of both budding yeast and the nematode worm Caenorhabditis elegans, and mammalian SIRT1 might increase longevity by shifting FOXO dependent responses away from cell death and towards cell survival.

TL;DR: The focus has shifted from studying the effects of single gene mutations with ubiquitous effects to finding interventions that alter IIS in specific tissues and at specific stages in the life history of the fruitfly in order to elucidate the signalling pathways at work and the mechanisms by which alterations in the IIS pathway can extend lifespan.

TL;DR: Although DR extends lifespan of flies in the absence of d FOXO, the presence of active dFOXO modulates the response to DR, possibly by modifying expression of its target genes, and may therefore mediate the normal response toDR.

TL;DR: The results suggest that there is evolutionary divergence in the downstream mechanisms that mediate the effects of IIS and imply that in Drosophila, additional factors act alongside dFOXO to produce IIS‐dependent responses in body size, fecundity, and oxidative stress resistance and that these phenotypes are not causal in IIS-mediated extension of lifespan.