Sci. STKE, 8 February 2000
Behavior and Metabolism Serotonin-Deficient Worms
Serotonin regulates several biochemical pathways that direct behavioral outcomes in organisms. Usually, the necessity for serotonin has been demonstrated through the expression of singly mutated serotonin receptor subunits. However, functional serotonin receptors can still exist that do not incorporate the mutant receptor subunit, thereby potentially masking serotonin-dependent pathways. Sze et al. report the generation of functional biosynthetic serotonin deficiency in Caenorhabditis elegans by knocking out its tryptophan hydroxylase gene. Mutant worms were viable but exhibited abnormal behavior with regard to food perception and ingestion as demonstrated by decreased rates of feeding. Additionally, they store large reserves of fat. In C. elegans, serotonin impinges upon both the insulin-like and DAF-7 (Transforming Growth Factor β) signal pathways, which are required to regulate its metabolism and development. Sze et al. also observed that disruption of serotonin biosynthesis in C. elegans decreased the expression of DAF-7. Thus, serotonin-deficiency leads to abnormal food intake and metabolic disruption as a result of defective DAF-7 and insulin-like signaling in worms.
Sze, J.Y., Victor, M., Loer, C., Shi, Y., and Ruvkun, G. (2000) Food and metabolic signalling defects in a Caenorhabditis elegans serotonin-synthesis mutant. Nature 403: 560-564. [Online Journal]
Citation: Serotonin-Deficient Worms. Sci. STKE 2000, tw4 (2000).
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