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Fig. 4. Effects of the TRPV genes on 5HT-modulated behaviors. (A) Dauer metabolic arrest. Similar to the tph-1 deletion mutation, the TRPV mutations and another ADF-5HT deficit mutation, nss-1(yz12), enhance Dauer arrest of the daf-7(e1372) mutation at the 15°C growth temperature. This enhanced Dauer phenotype is suppressed by a deletion mutation of the daf-16 gene, which is a negative target of the DAF-2/insulin signaling pathway. We noticed that daf-7;osm-9;daf-16 animals grow slower and sometimes form Dauer-like larvae but then go on to develop to adults, suggesting that the daf-2 pathway may not be the only signaling affected in the mutant. The Plin-11::osm-9(+) transgene was carried as an extrachromosomal array, only the animals carrying the transgenic marker were scored. The osm-9(yz6) (n=956), or ocr-2(yz5) (n=346) mutants alone do not form Dauers under the assay condition. (B) Egg-laying behavior. Unlike tph-1 mutant animals, the TRPV mutant adults do not accumulate a large amount of fertilized eggs in the uterus. (C) Feeding behavior. tph-1 mutant animals have no detectable 5HT in any serotonergic neuron and exhibit slower pharyngeal pumping rates, whereas animals bearing a mutation in the TRPV genes pump at rates similar to wild-type animals. The feeding and egg-laying behavior represents the summary of two independent trials, ten animals/strain/trial. The Dauer assay is the summary of three independent trials, each in duplicate. Error bars indicate the s.e.m.

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