Fat cells reactivate quiescent neuroblasts via TOR and glial insulin relays in Drosophila

Rita Sousa-Nunes, Lih Ling Yee and Alex P. Gould ()
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Rita Sousa-Nunes: Medical Research Council National Institute for Medical Research, The Ridgeway, Mill Hill
Lih Ling Yee: Medical Research Council National Institute for Medical Research, The Ridgeway, Mill Hill
Alex P. Gould: Medical Research Council National Institute for Medical Research, The Ridgeway, Mill Hill

Nature, 2011, vol. 471, issue 7339, 508-512

Abstract: Nerve progenitors hungry for action The availability of nutrients prompts quiescent neural stem cells (neuroblasts) in Drosophila larvae to begin to divide. A study of the mechanism linking diet to stem-cell behaviour has identified a relay mechanism regulating this nutritional checkpoint. Specific insulin-like peptides produced within the brain by glia — non-neuronal cells with various physical and biochemical support roles — form a bridge from the amino-acid/TOR-dependent signal derived from the fat body to PI3K/TOR signalling in neuroblasts to induce exit from quiescence.

Date: 2011
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DOI: 10.1038/nature09867

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