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First published online 3 March 2004
doi: 10.1242/dev.01047
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Department of Anatomy and Neurobiology, College of Medicine, University of California Irvine, Irvine, CA 92697-4040, USA
* Author for correspondence (e-mail: jsze{at}uci.edu)
Accepted 19 December 2003
Serotonin (5HT) is a pivotal signaling molecule that modulates behavioral
and endocrine responses to diverse chemical and physical stimuli. We report
cell-specific regulation of 5HT biosynthesis by transient receptor potential V
(TRPV) ion channels in C. elegans. Mutations in the TRPV genes
osm-9 or ocr-2 dramatically downregulate the expression of
the gene encoding the 5HT synthesis enzyme tryptophan hydroxylase
(tph-1) in the serotonergic chemosensory neurons ADF, but neither the
mutation nor the double mutation of both channel genes affects other types of
serotonergic neurons. The TRPV genes are expressed in the ADF neurons but not
in other serotonergic neurons, and act cell-autonomously to regulate a
neuron-specific transcription program. Whereas in olfactory neurons OSM-9 and
OCR-2 function is dependent on ODR-3 G
, the activity of ODR-3 or two
other G
proteins expressed in the ADF neurons is not required for
upregulating tph-1 expression, thus the TRPV ion channels in
different neurons may be regulated by different mechanisms. A gain-of-function
mutation in CaMKII UNC-43 partially suppresses the downregulation of
tph-1 in the TRPV mutants, thus CaMKII may be an effector of the TRPV
signaling. Mutations in the TRPV genes cause worms developmentally arrest at
the Dauer stage. This developmental defect is due in part to reduced 5HT
inputs into daf-2/insulin neuroendocrine signaling.
Key words: C. elegans, Transcription, Serotonin biosynthesis, TRPV ion channels, Metabolic control
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