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Neuron. 2002 Dec 19;36(6):1079-89.

The cyclic GMP-dependent protein kinase EGL-4 regulates olfactory adaptation in C. elegans.

Author information

1
Howard Hughes Medical Institute, Programs in Developmental Biology, Neuroscience, and Genetics, Department of Anatomy, The University of California, San Francisco, San Francisco, CA 94143, USA.

Abstract

Prolonged odor exposure causes a specific, reversible adaptation of olfactory responses. A genetic screen for negative regulators of olfaction uncovered mutations in the cGMP-dependent protein kinase EGL-4 that disrupt olfactory adaptation in C. elegans. G protein-coupled olfactory receptors within the AWC olfactory neuron signal through cGMP and a cGMP-gated channel. The cGMP-dependent kinase functions in AWC neurons during odor exposure to direct adaptation to AWC-sensed odors, suggesting that adaptation is a cell intrinsic process initiated by cGMP. A predicted phosphorylation site on the beta subunit of the cGMP-gated channel is required for adaptation after short odor exposure, suggesting that phosphorylation of signaling molecules generates adaptation at early time points. A predicted nuclear localization signal within EGL-4 is required for adaptation after longer odor exposure, suggesting that nuclear translocation of EGL-4 triggers late forms of adaptation.

PMID:
12495623
DOI:
10.1016/s0896-6273(02)01066-8
[Indexed for MEDLINE]
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