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 serotonin (5-HT) dependent. Animals mutant for the 5-HT reuptake transporter
mod-5 slow even more than wild-type animals. Additionally,
mod-5 animals are hypersensitive to exogenous 5-HT. To identify additional genes involved in 5-HT signaling and possibly the enhanced slowing response, we screened for suppressors of this 5-HT hypersensitivity. We screened 46,200 haploid genomes using Mos1 transposon mutagenesis (Bessereau et al. Nature, 413: 70-74, 2001). Four strong suppressors were identified. Two contain insertions in genes previously known to suppress
mod-5 for both the exogenous 5-HT hypersensitivity and the hyperenhanced slowing response. One of these suppressors is an allele of
mod-1, which encodes a 5-HT-gated chloride channel, and the other is an allele of
goa-1, a predicted alpha subunit of a heterotrimeric G-protein. Four transposon insertions have been identified on chromosome I in the strain carrying the third suppressor,
n4094. Four transposon insertions have also been identified in the strain carrying the fourth suppressor,
n4095. Experiments are underway to determine which of these insertions, if any, causes suppression of the 5-HT hypersensitivity of
mod-5. We are also working to define neural circuits through which both
mod-5 and suppressors of
mod-5 act to affect the hyperenhanced slowing response. Using antibodies raised against MOD-5 protein, we have identified several head neurons in which MOD-5 expression can be seen. Additionally, a translational
mod-1::rfp reporter has been constructed (by Eric Miska), and we are currently identifying the cells in which it is expressed.