학술논문

Dietary restriction and the transcription factor clock delay eye aging to extend lifespan in Drosophila Melanogaster
Document Type
article
Source
Nature Communications. 13(1)
Subject
Biological Sciences
Biomedical and Clinical Sciences
Ophthalmology and Optometry
Sleep Research
Nutrition
Aging
Eye Disease and Disorders of Vision
Neurosciences
Genetics
1.1 Normal biological development and functioning
Underpinning research
Eye
Animals
Circadian Rhythm
Drosophila Proteins
Drosophila melanogaster
Gene Expression Regulation
Longevity
Transcription Factors
Language
Abstract
Many vital processes in the eye are under circadian regulation, and circadian dysfunction has emerged as a potential driver of eye aging. Dietary restriction is one of the most robust lifespan-extending therapies and amplifies circadian rhythms with age. Herein, we demonstrate that dietary restriction extends lifespan in Drosophila melanogaster by promoting circadian homeostatic processes that protect the visual system from age- and light-associated damage. Altering the positive limb core molecular clock transcription factor, CLOCK, or CLOCK-output genes, accelerates visual senescence, induces a systemic immune response, and shortens lifespan. Flies subjected to dietary restriction are protected from the lifespan-shortening effects of photoreceptor activation. Inversely, photoreceptor inactivation, achieved via mutating rhodopsin or housing flies in constant darkness, primarily extends the lifespan of flies reared on a high-nutrient diet. Our findings establish the eye as a diet-sensitive modulator of lifespan and indicates that vision is an antagonistically pleiotropic process that contributes to organismal aging.