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Sci. Signal., 29 March 2011
Vol. 4, Issue 166, p. ec92
[DOI: 10.1126/scisignal.4166ec92]

EDITORS' CHOICE

Development From Fat Body to Glia to Neuroblasts

Elizabeth M. Adler

Science Signaling, AAAS, Washington, DC 20005, USA

Quiescent neuroblasts in the larval Drosophila central nervous system are reactivated to enter the cell cycle in response to dietary amino acids; in vitro analyses have also implicated signals from the fat body (a hepatic- and adipose-like tissue that senses amino acid nutrient status to regulate larval growth) in neuroblast reactivation. Sousa-Nunes et al. showed that neuroblast reactivation was inhibited in Drosophila larvae bearing a dominant-negative mutant that blocked vesicular trafficking in the fat body, implicating a fat-body–derived signal (FDS) in the in vivo response as well. A fat-body pathway involving the amino acid transporter Slimfast (SLIF) and target of rapamycin (TOR) signaling leads to production of a systemic signal that stimulates larval growth. Various genetic manipulations, including fat-body–specific knockdown of the gene encoding SLIF or expression of genes encoding the TOR inhibitors tuberous sclerosis complex 1 and 2, indicated that the FDS mediating neuroblast exit from quiescence also depended on a fat-body SLIF-TOR pathway. Moreover, genetic manipulation of neuroblast signaling indicated that neuroblast reactivation response to the FDS involved the interconnected TOR and phosphatidylinositol 3-kinase (PI3K) signaling pathways. Expression in neuroblasts of dominant-negative or constitutively activated forms of the insulin-like receptor (InR) implicated InR signaling in neuroblast reactivation, and analyses of larvae deficient in various insulin-like peptides (ILPs) implicated certain ILPs in regulating the timing of neuroblast reactivation. Brain median neurosecretory cells (mNSCs) secrete ILPs into the hemolymph to regulate larval growth in response to a FDS; however, overexpression of ILPs in mNSCs failed to reactivate neuroblasts during nutrient restriction, and mNSC manipulations that altered body growth in fed larvae failed to affect neuroblast reactivation. Transgenic analyses indicated that ILPs were also expressed in some glia, and overexpression of ILPs in neurons or glia—in conjunction with neuron- or glia-specific inhibition of vesicular trafficking—implicated glial-derived ILPs in neuroblast reactivation but not in body growth. Thus, the authors propose that a FDS to glia stimulates their production and release of ILPs to stimulate neuroblast reactivation, providing a functionally distinct pool of ILPs from those released by mNSCs to regulate body growth. A separate study by Chell and Brand similarly implicated glial ILP signaling in Drosophila neuroblast reactivation.

R. Sousa-Nunes, L. L. Yee, A. P. Gould, Fat cells reactivate quiescent neuroblasts via TOR and glial insulin relays in Drosophila. Nature 471, 508–512 (2011). [PubMed]

J. M. Chell, A. H. Brand, Nutrition-responsive glia control exit of neural stem cells from quiescence. Cell 143, 1161–1173 (2010). [PubMed]

Citation: E. M. Adler, From Fat Body to Glia to Neuroblasts. Sci. Signal. 4, ec92 (2011).



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