FB2026_03 , released September 17, 2026
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Citation
Broughton, S.J., Slack, C., Alic, N., Metaxakis, A., Bass, T.M., Driege, Y., Partridge, L. (2010). DILP-producing median neurosecretory cells in the Drosophila brain mediate the response of lifespan to nutrition.  Aging Cell 9(3): 336--346.
FlyBase ID
FBrf0211116
Publication Type
Research paper
Abstract
Dietary restriction extends lifespan in diverse organisms, but the gene regulatory mechanisms and tissues mediating the increased survival are still unclear. Studies in worms and flies have revealed a number of candidate mechanisms, including the target of rapamycin and insulin/IGF-like signalling (IIS) pathways and suggested a specific role for the nervous system in mediating the response. A pair of sensory neurons in Caenorhabditis elegans has been found to specifically mediate DR lifespan extension, but a neuronal focus in the Drosophila nervous system has not yet been identified. We have previously shown that reducing IIS via the partial ablation of median neurosecretory cells in the Drosophila adult brain, which produce three of the seven fly insulin-like peptides, extends lifespan. Here, we show that these cells are required to mediate the response of lifespan to full feeding in a yeast dilution DR regime and that they appear to do so by mechanisms that involve both altered IIS and other endocrine effects. We also present evidence of an interaction between these mNSCs, nutrition and sleep, further emphasising the functional homology between the DILP-producing neurosecretory cells in the Drosophila brain and the hypothalamus of mammals in their roles as integration sites of many inputs for the control of lifespan and behaviour.
PubMed ID
PubMed Central ID
PMC4467032 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Aging Cell
    Title
    Aging Cell
    Publication Year
    2002-
    ISBN/ISSN
    1474-9718 1474-9728
    Data From Reference
    Alleles (2)
    Genes (4)
    Human Disease Models (1)
    Transgenic Constructs (2)