Epigenetic mechanisms of dietary restriction induced aging in Drosophila.

Aging is a long-standing problem that people are always interested in. Thus, it is critical to understand the underlying molecular mechanisms in aging and explore the most efficient method to extend life expectancy. To achieve this goal, a wide range of systems including cells, rodent models, budding yeast, worms and flies have been employed for decades. In recent years, the effect of dietary restriction (DR) on lifespan is in the prime focus. Although we have confirmed that reduced insulin and/or insulin-like growth factor (IGF) and the target of rapamycin (TOR) signaling can increase Drosophila lifespan; the precise molecular mechanisms and nutritional response landscape of diet-mediated aging is ambiguous. Epigenetic events have been considered as the major contributors to lifespan extension with response to DR. The role of DNA methylation in aging is well acknowledged in mammals and rodents where it has been shown to impact aging by regulating the transcription, though the mechanism of regulation is not limited to only transcription. In Drosophila, the contribution of methylation during DR in aging is definitely less explored. In this review, we will update the advances in mechanisms of DR, with a particular focus on methylation as an upcoming target for aging studies and discuss Drosophila as a powerful model to understand mechanisms of aging with response to diet.