Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-657
Ikeya, T; Galic, M; Belawat, P; Nairz, K; Hafen, E (2002). Nutrient-dependent expression of insulin-like peptides from neuroendocrine cells in the CNS contributes to growth regulation in Drosophila. Current Biology, 12(15):1293-1300.
View at publisher
BACKGROUND: The insulin/IGF-1 signaling pathway controls cellular and organismal growth in many multicellular organisms. In Drosophila, genetic defects in components of the insulin signaling pathway produce small flies that are delayed in development and possess fewer and smaller cells as well as female sterility, reminiscent of the phenotypes of starved flies. RESULTS: Here we establish a causal link between nutrient availability and insulin-dependent growth. We show that in addition to the Drosophila insulin-like peptide 2 (dilp2) gene, overexpression of dilp1 and dilp3-7 is sufficient to promote growth. Three of the dilp genes are expressed in seven median neurosecretory cells (m-NSCs) in the brain. These m-NSCs possess axon terminals in the larval endocrine gland and on the aorta, from which DILPs may be released into the circulatory system. Although expressed in the same cells, the expression of the three genes is controlled by unrelated cis-regulatory elements. The expression of two of the three genes is regulated by nutrient availability. Genetic ablation of these neurosecretory cells mimics the phenotype of starved or insulin signaling mutant flies. CONCLUSIONS: These results point to a conserved role of the neuroendocrine axis in growth control in multicellular organisms.
221 downloads since deposited on 11 Feb 2008
43 downloads since 12 months
|Item Type:||Journal Article, refereed|
|Communities & Collections:||07 Faculty of Science > Institute of Zoology (former)|
|Dewey Decimal Classification:||570 Life sciences; biology
590 Animals (Zoology)
|Date:||6 August 2002|
|Deposited On:||11 Feb 2008 12:17|
|Last Modified:||05 Apr 2016 12:15|
Users (please log in): suggest update or correction for this item
Repository Staff Only: item control page