We have identified two genes predicted to encode potassium channels that negatively regulate C. elegans egg-laying behavior.
In one study we found that the mutation
n575, which defined the gene
egl-7 and confers a dominant egg-laying defect, is an allele of
unc-103.
unc-103 is predicted to encode the C. elegans ortholog of mammalian HERG and Drosophila seizure, cyclic nucleotide-gated voltage-sensitive potassium channels. The
n575 mutation affects the splice-acceptor site for exon 8 of
unc-103, resulting in the use of a cryptic splice acceptor 90 basepairs downstream. The predicted protein product of
unc-103(
n575) lacks a highly conserved 30 amino acid sequence adjacent to the cyclic nucleotide binding domain in the cytoplasmic COOH terminus of the channel. We isolated
n4328 as a dominant suppressor of the
n575 Egl phenotype and found that
n4328 n575 mutants harbor a missense mutation in the
unc-103 coding sequence in addition to the
n575 mutation. Gene-dosage studies indicate that
n575 is a gain-of-function allele of
unc-103. Loss-of-function alleles of
unc-103, including
unc-103(
n4328 n575), confer an Egg-laying constitutive (Egl-c) phenotype, suggesting that the wild-type function of
unc-103 is to inhibit egg-laying behavior.
In another study we isolated deletion alleles of
irk-1 and
irk-2, which are predicted to encode the C. elegans potassium channels most similar to G protein-gated potassium channels found in vertebrate nervous systems. We are interested in testing the possibility that G protein-gated potassium channels are effectors of G protein signaling pathways that control C. elegans egg-laying behavior. Mutants carrying a deletion allele of
irk-2 have normal egg-laying behavior, but mutants carrying an
irk-1 deletion allele are Egl-c. We will present our characterization of genetic interactions between irk deletion alleles and mutations that affect G protein signaling in the C. elegans egg-laying neuromusculature.