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Food experience-induced taste desensitization modulated by the Drosophila TRPL channel.

Nature neuroscience (2013-09-10)
Yali V Zhang, Rakesh P Raghuwanshi, Wei L Shen, Craig Montell
RESUMEN

Animals tend to reject bitter foods. However, long-term exposure to some unpalatable tastants increases acceptance of these foods. Here we show that dietary exposure to an unappealing but safe additive, camphor, caused the fruit fly Drosophila melanogaster to decrease camphor rejection. The transient receptor potential-like (TRPL) cation channel was a direct target for camphor in gustatory receptor neurons, and long-term feeding on a camphor diet led to reversible downregulation of TRPL protein concentrations. The turnover of TRPL was controlled by an E3 ubiquitin ligase, Ube3a. The decline in TRPL levels and increased acceptance of camphor reversed after returning the flies to a camphor-free diet long term. We propose that dynamic regulation of taste receptors by ubiquitin-mediated protein degradation comprises an important molecular mechanism that allows an animal to alter its taste behavior in response to a changing food environment.

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Sigma-Aldrich
(±)-Alcanfor, 96%
Sigma-Aldrich
(1R)-(+)-Camphor, 98%
Sigma-Aldrich
D-Camphor, ≥97%, FG
Sigma-Aldrich
(1S)-(−)-Camphor, 95%
Sigma-Aldrich
(±)-Alcanfor, ≥95.5%
Supelco
D-Camphor, Pharmaceutical Secondary Standard; Certified Reference Material
Sigma-Aldrich
(±)-Alcanfor, meets analytical specification of Ph. Eur., BP, racemic, ≥95% (GC)
Sigma-Aldrich
(±)-Alcanfor, purum, synthetic, ≥95.0% (GC)
Supelco
(−)-Camphor, analytical standard
(±)-Alcanfor, European Pharmacopoeia (EP) Reference Standard
(±)-Alcanfor, primary reference standard
Sigma-Aldrich
(±)-Alcanfor, SAJ first grade, ≥96.0%