Serotonin signaling in C. elegans

Wild-type animals that have been acutely food deprived slow their locomotory rate upon encountering bacteria more than do well-fed animals. This behavior, called the enhanced slowing response, is partly serotonin (5-HT) dependent. Animals mutant for the 5-HT reuptake transporter gene mod-5 slow even more than wild-type animals because endogenous 5-HT activity is potentiated. This behavior, called the hyperenhanced slowing response, can be suppressed by mutations in genes that encode proteins important for 5-HT signaling, like the 5-HT receptor encoded by mod-1 and the Ga subunit of a G protein encoded by goa-1. This ability to suppress indicates that these genes likely act downstream of or in parallel to one or more 5-HT synapse(s) that mediate(s) the enhanced slowing response. To find genes that play a role in 5-HT signaling, we screened for suppressors of the 5-HT hypersensitivity of mod-5. We found at least seven alleles of goa-i and at least two alleles of mod-1. This shows that our screen is able to target genes that play a role in endogenous 5-HT signaling. We identified two alleles of the FMRFamide-encoding gene fp-1, which was known to mediate paralysis in exogenous 5-HT. We showed that loss-of-function mutations in flp-1 confer an enhanced slowing response defect. We also identified an allele of abts-1, which encodes a bicarbonate transporter, and showed that it has defects in cholinergic signaling. We identified three mutants that show linkage to LG I, four to II, three to V and one to X, most of which display defects consistent with a role in 5-HT signaling.

Department dc:contributor.department

Massachusetts Institute of Technology. Dept. of Biology.

Grantor dc:publisher

Massachusetts Institute of Technology

Year dc:date.issued

2007

Author dc:creator

• Gustafson, Megan Alyse

Advisor dc:contributor.advisor

• H. Robert Horvitz.

• Biology.

Statement dc:rights

• M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.

Licence dc:rights.uri

• http://dspace.mit.edu/handle/1721.1/7582

Language dc:language.iso

eng

Handle dc:identifier.uri

http://hdl.handle.net/1721.1/40957

OAI identifier oai:identifier

oai:dspace.mit.edu:1721.1/40957