Help Privacy Policy Disclaimer
  Advanced SearchBrowse




Journal Article

Neuronal Control of Metabolism through Nutrient-Dependent Modulation of Tracheal Branching.


Linneweber,  Gerit
Max Planck Society;

Jacobson,  Jake
Max Planck Society;

Busch,  Karl Emanuel
Max Planck Society;

Hudry,  Bruno
Max Planck Society;

Christov,  Christo P.
Max Planck Society;

Dormann,  Dirk
Max Planck Society;

Otani,  Tomoki
Max Planck Society;


Knust,  Elisabeth
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

Miguel-Aliaga,  Irene
Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available

Linneweber, G., Jacobson, J., Busch, K. E., Hudry, B., Christov, C. P., Dormann, D., et al. (2014). Neuronal Control of Metabolism through Nutrient-Dependent Modulation of Tracheal Branching. Cell, 156(1-2), 69-83.

Cite as: https://hdl.handle.net/21.11116/0000-0001-05CF-1
During adaptive angiogenesis, a key process in the etiology and treatment of cancer and obesity, the vasculature changes to meet the metabolic needs of its target tissues. Although the cues governing vascular remodeling are not fully understood, target-derived signals are generally believed to underlie this process. Here, we identify an alternative mechanism by characterizing the previously unrecognized nutrient-dependent plasticity of the Drosophila tracheal system: a network of oxygen-delivering tubules developmentally akin to mammalian blood vessels. We find that this plasticity, particularly prominent in the intestine, drives-rather than responds to-metabolic change. Mechanistically, it is regulated by distinct populations of nutrient- and oxygen-responsive neurons that, through delivery of both local and systemic insulin- and VIP-like neuropeptides, sculpt the growth of specific tracheal subsets. Thus, we describe a novel mechanism by which nutritional cues modulate neuronal activity to give rise to organ-specific, long-lasting changes in vascular architecture.