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Comments on Juang, Bi-Tzen et al. (2009) International Worm Meeting "HPL-2 and MUT-7 in odor-adaptation of the AWC neuron." (0)
Overview
Juang, Bi-Tzen, & L'Etoile, Noelle (2009). HPL-2 and MUT-7 in odor-adaptation of the AWC neuron presented in International Worm Meeting. Unpublished information; cite only with author permission.
A sensory neuron must be able to respond to signals from the environment and to either attenuate or amplify its responsiveness as a function of experience. C. elegans relies extensively upon its sense of smell to locate food, thus, survival requires that a worm is able to ignore (adapt to) odors that are not associated with food. We exploit the ability of the genetically tractable, anatomically simple nematode to adapt to persistent profitless odors in order to examine the molecular mechanisms underlying neuronal plasticity. In previous work we found that long-term adaptation requires nuclear translocation of a cGMP-dependent protein kinase (EGL-4) in the AWC olfactory neuron (Lee et al., submitted). Here we show that proteins within the RNA-induced transcriptional silencing (RITS) pathway may be targets of EGL-4 in the nucleus. Though RNAi has been well characterized in C. elegans development, our studies may be the first to demonstrate a role for this process for the plasticity of the adult sensory neuron. We screened through all known RNAi defective mutants that are also able to chemotax for those that also fail to adapt to AWC-sensed odors. We found that the Histone H3 K9 methyl binding protein HPL-2 and the RNAase III MUT-7 are both required within the AWC neuron at the time of odor exposure for proper odor-adaptation. From our genetic analysis, we found that HPL-2 and MUT-7 are likely to work in the same pathway to promote adaptation. We are testing the hypothesis that HPL-2 and/or MUT-7 are phosphorylated by EGL-4 in response to odor stimulation. Histone modification has been shown to be important for memory formation in mice (Nature 447:178-183). To analyze the effect of histone modification in maintaining neuronal plasticity, we examined that the H3 K4 histone methyltransferase SET-2 and found that it antagonizes the functions of HPL-2 and MUT-7 in olfactory adaptation. Our work opens up the possibility that this olfactory memory formation is dependent on chromatin changes and is actually initiated or maintained by small non-coding RNAs.