Three sets of C. elegans</I> sensory neurons, including the ASH neurons, are responsible for an animals ability to detect light touch to the nose (nose touch). These neurons synapse onto a series of interneurons critical for locomotion and direction of movement. We have previously described cloning and characterization of
rt144, a mutation in the kinase domain of protein kinase C-1 (
pkc-1).
rt144 reduces an animals nose touch response to ~50% (WBPaper26055). Additional
pkc-1 alleles, including the
ok563 deletion allele, have similar nose touch defects, suggesting that these alleles cause severe loss of function defects. Previous reports have demonstrated that
pkc-1 acts in sensory neurons for sensory transduction (WBPaper25220). To determine the
pkc-1 </I>cellular site of action for nose touch response, we generated rescue constructs expressing
pkc-1</I> cDNA either in the ASH sensory neurons or the interneurons of
pkc-1(
ok563) animals. Surprisingly, we find that only the
glr-1</I> promoter rescue construct restores wild type nose touch response, suggesting that
pkc-1 is required in the interneurons. The AMPA/kainate glutamate receptors
glr-1</I> and
glr-2 </I>are expressed in the interneurons and are required for nose touch response. To investigate the genetic relationship between these receptors and
pkc-1</I>, we constructed double mutant strains as well as examined expression of GLR-1::GFP in
pkc-1(
ok563)</I> animals. Loss of
pkc-1</I> did not alter nose touch response in animals lacking
glr-1</I> or
glr-2</I> and GLR-1::GFP expression in the interneurons was unchanged in
pkc-1</I> animals. We conclude that although
pkc-1</I> and glutamate receptors may act in the same pathway,
pkc-1</I> activity does not affect localization of GLR-1. Mammalian tissue culture studies have shown that PKC activates the MAP kinase signaling pathway through its interactions with the MAPKKK Raf-1. Members of the MAPK signaling pathway, including
lin-45</I> raf, are required for AWA and AWC mediated olfaction (WBPaper3955), and a
lin-45::GFP</I> reporter is expressed in a few unidentified head neurons(WBPaper10955). We examined the behavior of two mutant strains,
lin-45(
sy96) </I>and
lin-45(
n2018)</I>. Both of these hypomorphic alleles reduced nose touch response to ~50%. Knockdown of
lin-45</I> in the interneurons also resulted in a nose touch defect, suggesting that
pkc-1</I> and
lin-45</I> may act in the same cells. We are currently examining whether
pkc-1</I> and
lin-45</I> act in the same pathway and if other members of the MAP kinase pathway play roles in nose touch response. This analysis will provide new insights on the downstream targets of
pkc-1</I> signaling in C. elegans</I> behavior.