For worms, recognition towards certain odors and foods is a fundamental behavior in life. It is necessary to distinguish between profitless and beneficial volatile odors for survival. Odors can be sensed by sensory neurons within the Caenorhabditis elegan head region. Certain odors such as benzaldehyde, butanone, and isoamyl alcohol can be sensed by specific neurons, like the AWC. We are investigating the signaling pathway associated with the behavioral pattern of the worm when exposed to a volatile odor. Adaptation refers to when an organism learns to ignore a persistent, profitless odor. A PKG is a serine/threonine specific kinase activated by cGMP. We have identified
egl-4 as a Caenorhabditis elegans PKG and have shown that long-term adaptation results in the translocation of EGL-4, from the AWC-cytoplasm to the AWC-nucleus. It is known that in an
egl-4 null mutant, adaptation behavior becomes defective. This suggests that adaptation is a cell intrinsic process initiated by cGMP (L'Etoile et al., Neuron, 2002). Because EGL-4 seems to be crucial in the adaptation to volatile odors, we wondered if there was another PKG. A second cGMP dependent protein kinase (PKG) was recently identified within the Caenorhabditis elegans genome. It is encoded by C09G4.2. We would like to determine if C09G4.2 is involved in AWC-mediated behaviors. In order to examine the role of this PKG, we are examining AWC-mediated behavior in
ok966 and
tm3878 deletion mutant strains. We have conducted chemotaxis, adaptation, and food block assays in order to check the role of this PKG in sensory neurons.