Disrupting a clock protein shortens fly life on a high-fat diet
Experiments in male fruit flies found that disrupting one clock protein increased immune gene activity in a metabolic tissue, unlike disrupting its partner.
Limit: The experiments did not measure whether immune changes caused the shorter lifespan
Edited by Boris Djordjevic · AgingResearch.News
In experiments in male fruit flies (Drosophila melanogaster), aging and a high-fat diet weakened daily activity rhythms. Researchers monitored molecular clocks in living flies fed standard or lard-enriched food. Clocks in the fat body, a tissue that regulates metabolism and immunity, weakened with age and diet. Brain clock cells resisted dietary stress but declined with age.
The team also disrupted individual clock components in the fat body and tracked survival throughout life. Disrupting CLOCK, a protein that helps control daily gene activity, shortened lifespan on high-fat food compared with genetic controls, but not on standard food. Disrupting three other clock components did not shorten lifespan. CLOCK disruption also increased gene activity for antimicrobial peptides, molecules that fight microbes. Disrupting its partner protein CYCLE did not, despite weakening molecular rhythms similarly.
Why it matters
The authors suggest that the distinct roles of individual clock proteins have implications for understanding age-related inflammation and metabolic disease.
Caveats
The experiments were in male flies and did not establish whether the immune changes caused the shorter lifespan. This preprint has not been peer-reviewed.
The paper
Fat body CLOCK restrains innate immunity and maintains survival under dietary stress in Drosophila
Rutgers, The State University of New Jersey
bioRxiv, Jul 21, 2026, Open access, Preprint, not peer-reviewed
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