A nutrient sensor mechanism controls Drosophila growth

被引:610
作者
Colombani, J
Raisin, S
Pantalacci, S
Radimerski, T
Montagne, J
Léopold, P
机构
[1] Inst Signaling Dev Biol & Canc Res, UMR 6543, CNRS, F-06108 Nice 2, France
[2] Friedrich Miescher Inst, CH-4058 Basel, Switzerland
关键词
D O I
10.1016/S0092-8674(03)00713-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Organisms modulate their growth according to nutrient availability. Although individual cells in a multicellular animal may respond directly to nutrient levels, growth of the entire organism needs to be coordinated. Here, we provide evidence that in Drosophila, coordination of organismal growl, originates from the fat body, an insect organ that retains endocrine and storage functions of the vertebrate liver. In a genetic screen for growth modifiers, we identified slimfast, a gene that encodes an amino acid transporter. Remarkably, downregulation of slimfast specifically within the fat body causes a global growth defect similar to that seen in Drosophila raised under poor nutritional conditions. This involves TSC/TOR signaling in the fat body, and a remote inhibition of organismal growth via local repression of P13-kinase signaling in peripheral tissues. Our results demonstrate that the fat body functions as a nutrient sensor that restricts global growth through a humoral mechanism.
引用
收藏
页码:739 / 749
页数:11
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